pituitrin and Hemorrhage

The role of corticosteroid therapy in patients with cardiac arrest (CA) is uncertain. We aimed to evaluate the efficacy and safety of corticosteroid therapy in CA patients.. Randomised controlled trials were identified using PubMed, EMBASE, Cochrane Central Register of Controlled Trials, the Chinese National Knowledge Infrastructure and the Chinese Biomedical Literature Database. The primary outcome was overall survival. Secondary outcomes were positive neurological status and probability of sustained restoration of spontaneous circulation (ROSC). Complications were infection and bleeding. Given the significant heterogeneity across previous studies, combining the data using meta-analysis was deemed not appropriate.. Five studies (551 patients) met the criteria. Two studies of co-intervention therapy (corticosteroid, vasopressin and epinephrine protocol) found that this approach could benefit in-hospital CA patient survival rates at hospital discharge, improve neurological function at hospital discharge and yield sustained ROSC rate. However, further two studies failed to demonstrate that corticosteroid therapy alone could improve survival and neurological outcomes among CA patients. Additionally, corticosteroid therapy did not increase the risk of infection and bleeding.. Due to the inherent limitations of the studies in this review, we have not been able to reach definitive conclusions. Larger-scale and better-designed studies are therefore recommended, to further evaluate the potential and rational use of corticosteroid therapy in CA patients.

Topics: Cardiopulmonary Resuscitation; Drug Therapy, Combination; Epinephrine; Glucocorticoids; Heart Arrest; Hemorrhage; Hospital Mortality; Humans; Infections; Randomized Controlled Trials as Topic; Risk Assessment; Survival Rate; Treatment Outcome; Vasopressins

Uncontrolled elevation in plasma potassium within minutes of rapid blood volume loss is associated with mortality and distinguishes nonsurvivors of severe hemorrhage from survivors. In a pig model of severe hemorrhage, we discovered that along with a sharp increase in plasma potassium coincident with a shut down of urine flow, nonsurvivors also had an insufficient vasopressin response to hemorrhage. In contrast, survivors did have elevated vasopressin levels in response to hemorrhage and maintained plasma potassium within normal limits. While it has been demonstrated for some time that vasopressin can influence secretion of potassium in the distal nephron, the magnitude of this effect and conditions under which this contributes to physiological modulation of potassium excretion has yet to be defined. In this review, we assess the evidence that would suggest that vasopressin plays a key role in modulating potassium excretion and is important in the regulation of potassium homeostasis during hemorrhage.

Topics: Animals; Hemorrhage; Homeostasis; Hypotension; Potassium; Swine; Vasopressins

Portal hypertension is an increase in pressure in the portal vein and its tributaries. It is defined as a portal pressure gradient (the difference in pressure between the portal vein and the hepatic veins) greater than 5 mm Hg. Although this gradient defines portal hypertension, a gradient of 10 mm Hg or greater defines clinically significant portal hypertension, because this pressure gradient predicts the development of varices, decompensation of cirrhosis, and hepatocellular carcinoma. The most direct consequence of portal hypertension is the development of gastroesophageal varices that may rupture and lead to the development of variceal hemorrhage. This article reviews the pathophysiologic bases of the different pharmacologic treatments for portal hypertension in patients with cirrhosis and places them in the context of the natural history of varices and variceal hemorrhage.

Topics: Adrenergic beta-Antagonists; Fibrosis; Hemorrhage; Humans; Hypertension, Portal; Liver; Randomized Controlled Trials as Topic; Somatostatin; Varicose Veins; Vasoconstrictor Agents; Vasodilator Agents; Vasopressins

The vasopressin system is complex and interacts with the central nervous, cardiovascular, renal, and hematological systems. Vasopressin plays an important role in the control of blood osmolarity and vascular tone, but is also involved in many other physiological events, which are mediated mainly via three types of vasopressin receptor: V1R, V2R, and V3R. V1R primarily mediate the vascular, and V2R the aquaretic, effects of vasopressin. Vasopressin may also interact with other receptors, like adrenergic and angiotensin-II receptors, or with distinct biological pathways, including those of nitric oxide and the K(ATP) channel. There are numerous clinical situations where vasopressin receptor modulators (agonists or antagonists) could be used. Currently, vasopressin and terlipressin are most commonly used to stimulate V1R in vasodilatory shock and cardiac arrest, while desmopressin, a synthetic analogue of vasopressin, acts on V2R; but new molecules are becoming available in the treatment of inappropriate antidiuretic hormone (ADH) secretion.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Brain Diseases; Cardiovascular Diseases; Clinical Trials as Topic; Drugs, Investigational; Hemorrhage; Humans; Inappropriate ADH Syndrome; Receptors, Vasopressin; Skin Diseases; Vasopressins

Severely septic patients continue to experience excessive morbidity and mortality despite recent advances in critical care. Although significant resources have been invested in new treatments, almost all have failed to improve outcomes. An improved understanding of sepsis pathophysiology, including the complex interactions between inflammatory, coagulation, and fibrinolytic systems, has accelerated the development of novel treatments. Recombinant human activated protein C (rhAPC), or drotrecogin alfa (activated) (DAA), is currently the only US Food and Drug Administration (FDA)-approved medicine for the treatment of severe sepsis, and only in patients with a high risk of death. This review will discuss the treatment of severe sepsis, focusing on recent discoveries and unresolved questions about DAA's optimal use. Increasing pharmacological experience has generated enthusiasm for investigating medicines already approved for other indications as treatments for severe sepsis. Replacement doses of hydrocortisone and vasopressin may reduce mortality and improve hypotension, respectively, in a subgroup of patients with catecholamine-refractory septic shock. In addition to discussing these new indications, this review will detail the provocative preliminary data from four promising treatments, including two novel modalities: antagonizing high mobility group box protein and inhibiting tissue factor (TF). Observational data from the uncontrolled administration of heparin or statins in septic patients will also be reviewed.

Topics: Adrenal Cortex Hormones; Anti-Infective Agents; Anti-Inflammatory Agents; Anticoagulants; Antidiuretic Agents; Drug Administration Schedule; Drug Therapy; Hemorrhage; Heparin; HMGB1 Protein; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Patient Selection; Protein C; Recombinant Proteins; Sepsis; Severity of Illness Index; Thromboplastin; Treatment Outcome; Vasopressins

Bleeding occurs in up to 10% of patients with advanced cancer. It can present in many different ways. This article provides a qualitative review of treatment options available to manage visible bleeding. Local modalities, such as hemostatic agents and dressings, radiotherapy, endoscopic ligation and coagulation, and transcutaneous arterial embolization, are reviewed in the context of advanced cancer, as are systemic treatments such as vitamin K, vasopressin/desmopressin, octreotide/somatostatin, antifibrinolytic agents (tranexamic acid and aminocaproic acid), and blood products. Considerations at the end of life are described.

Topics: Antifibrinolytic Agents; Bandages; Blood Transfusion; Endoscopy; Hemorrhage; Hemostatic Techniques; Humans; Neoplasms; Radiotherapy; Somatostatin; Terminal Care; Vasopressins; Vitamin K

The antidiuretic hormone (ADH) vasopressin is a simple peptide hormone with a number of complex, essential physiological actions. It is becoming clear that this hormone is developing an important therapeutic role in a number of different conditions. These include vasodilatory shock due to sepsis or cardiac surgery, cardiac arrest, and prolonged/excessive bleeding caused by, for example, variceal haemorrhage. This article reviews the physiology of ADH relevant to these actions and scrutinises the evidence for its therapeutic applications.

Topics: Heart Arrest; Hemorrhage; Hemostatics; Humans; Renal Agents; Shock; Thoracic Surgery; Vasoconstrictor Agents; Vasopressins

Studies of octreotide have not demonstrated a consistent benefit in efficacy or safety compared with conventional therapies. This study statistically pooled existing trials to evaluate the safety and efficacy of octreotide for esophageal variceal hemorrhage.. We identified randomized trials of octreotide for variceal hemorrhage from computerized databases, scientific meeting abstracts, and the manufacturer of octreotide. Blinded reviewers abstracted the data, and a meta-analysis was performed.. Octreotide improved control of esophageal variceal hemorrhage compared with all alternative therapies combined (relative risk [RR], 0.63; 95% confidence interval [CI], 0.51-0.77); vasopressin/terlipressin (RR, 0.58; 95% CI, 0.42-0.81); or no additional intervention/placebo (among patients that received initial sclerotherapy/banding before randomization) (RR, 0.46; 95% CI, 0.32-0.67). Octreotide had comparable efficacy to immediate sclerotherapy for control of bleeding (RR, 0.94; 95% CI, 0.55-1.62), fewer major complications than vasopressin/terlipessin (RR, 0.31; 95% CI, 0.11-0.87), and a complication profile comparable to no intervention/placebo (RR, 1.06; 95% CI, 0.72-1.55). No specific alternative therapy demonstrated a mortality benefit.. These results favor octreotide over vasopressin/terlipressin in the control of esophageal variceal bleeding and suggest it is a safe and effective adjunctive therapy after variceal obliteration techniques. Trials are needed to determine the optimal dose, route, and duration of octreotide treatment.

Topics: Acute Disease; Esophageal and Gastric Varices; Hemorrhage; Hemostatics; Humans; Lypressin; Octreotide; Recurrence; Terlipressin; Vasopressins

Topics: Antifibrinolytic Agents; Cardiopulmonary Bypass; Deamino Arginine Vasopressin; Factor VIII; Hemorrhage; Humans; Platelet Transfusion; United Kingdom; Vasopressins; von Willebrand Factor

Topics: Adrenergic beta-Antagonists; Ascites; Carcinoma, Hepatocellular; Catheterization; Diuretics; Hemorrhage; Hepatic Encephalopathy; Humans; Hypertension, Portal; Liver Cirrhosis; Liver Neoplasms; Nitroglycerin; Peritonitis; Somatostatin; Vasopressins

A survey is given on the regulation of the formation of corticoliberin and of pro-opiomelanocortin and of ACTH, respectively, and on the significance of these compounds. The formation of pro-opiomelanocortin is furthered by corticoliberin, vasopressin, oxytocin and angiotensin II. Receptors for the binding of corticoliberin appear in numerous parts of the central nervous system. In various diseases the content of corticoliberin in the plasma and in certain tissues is changed. The inhibition of the ACTH secretion by glucocorticosteroids takes place via a decrease of the formation of corticoliberin and by a reduction of the equipment of the corticotrophic cells with receptors for its binding. The secretion of corticoliberin and of ACTH, respectively, is increased by loads, by hypoglycaemia, by blood losses, by hypoxia and by infections. In the glucocorticosteroid receptors there are 2 types with different affinity to cortisol and corticosterone.

Topics: Adrenocorticotropic Hormone; Angiotensin II; Corticotropin-Releasing Hormone; Hemorrhage; Humans; Hypoglycemia; Hypoxia; Infections; Oxytocin; Pro-Opiomelanocortin; Receptors, Cell Surface; Vasopressins

Antagonists of the vasopressor response to vasopressin (VP) have proved useful for probing the contributions of endogenous VP to cardiovascular regulation. Studies with such antagonists show that VP can exert substantial cardiovascular effects even when circulating levels are relatively low, as they are after moderate dehydration. Antagonists that also block antidiuretic responses to VP have recently become available. These promise to be equally useful for assessing the importance of VP in limiting water excretion under a variety of circumstances. Although many of the antagonists of the vasopressor response are relatively specific, the early antidiuretic antagonists were not. They block both vasopressor and antidiuretic receptors. Recently we have made progress in designing analogs that are more specific antagonists of the antidiuretic response. This suggests that it should be possible to produce specific antagonists of the antidiuretic response that would provide more incisive pharmacological probes and could become useful therapeutic agents.

Topics: Animals; Blood Pressure; Hemorrhage; Oxytocin; Rabbits; Rats; Rats, Inbred SHR; Receptors, Angiotensin; Receptors, Oxytocin; Receptors, Vasopressin; Urination; Vasopressins

The effects of changes in the composition and/or the volume of the extracellular fluid on central receptors involved in the regulation of water balance are discussed. A review of results obtained in adults is given, followed by a discussion of possible roles for vasopressin during the neonatal period.

Topics: Angiotensin II; Animals; Blood Volume; Diuresis; Drinking; Extracellular Space; Female; Hemorrhage; Humans; Hypothalamus; Infant, Newborn; Labor, Obstetric; Osmolar Concentration; Pregnancy; Renin-Angiotensin System; Sodium; Thirst; Vasopressins; Water-Electrolyte Balance

Topics: Angiotensin II; Animals; Dogs; Hemorrhage; Humans; Hypertension; Male; Pituitary Gland; Posture; Rats; Renin; Renin-Angiotensin System; Sodium; Supraoptic Nucleus; Thirst; Vasoconstriction; Vasopressins

Topics: Animals; Arginine Vasopressin; Blood Pressure; Blood Volume; Cardiac Output; Catecholamines; Desoxycorticosterone; Diabetes Insipidus; Drug Interactions; Hemodynamics; Hemorrhage; Homeostasis; Humans; Hypertension; Immune Sera; Pressoreceptors; Rats; Rats, Brattleboro; Rats, Mutant Strains; Vascular Resistance; Vasopressins

Topics: Angiotensin II; Animals; Body Water; Brain; Circadian Rhythm; Drinking Behavior; Hemorrhage; Homeostasis; Limbic System; Nucleus Accumbens; Osmolar Concentration; Receptors, Angiotensin; Reticular Formation; Saline Solution, Hypertonic; Superior Colliculi; Taste; Tegmentum Mesencephali; Thirst; Vasopressins

Topics: Angiography; Arteriovenous Malformations; Catheterization; Embolization, Therapeutic; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Hemorrhage; Humans; Neoplasms; Regional Blood Flow; Vasopressins; Wounds and Injuries

Topics: Angiotensins; Catecholamines; Diabetes Mellitus; Hemorrhage; Hormones; Humans; Liver; Obesity; Phosphorylases; Shock; Vasopressins

The use of diagnostic and therapeutic angiography for postoperative bleeding which began with its application for bleeding following GI surgery can be ezpanded to almost all other areas of the body. Severe postoperative hemorrhage that previously required a second operation can now be successfully managed by the use of intraarterial or intravenous vasoconstrictors or transcatheter occlusion, thus significantly reducing patient morbidity and mortality. In those patients where a reexploration becomes necessary, diagnostic angiogarphy is a useful guide and helps to tailor the operative procedures.

Topics: Aged; Angiography; Catheterization; Embolization, Therapeutic; Esophageal Diseases; Gastrointestinal Hemorrhage; Gelatin; Hemorrhage; Hip; Humans; Intestine, Small; Kidney Diseases; Male; Pelvic Neoplasms; Postoperative Complications; Stomach Diseases; Tissue Adhesives; Vasopressins

Topics: Animals; Blood Volume; Copulation; Exocytosis; Female; Hemorrhage; Labor, Obstetric; Lactation; Male; Neurophysins; Neurosecretory Systems; Organoids; Oxytocin; Paraventricular Hypothalamic Nucleus; Pituitary Gland, Posterior; Pregnancy; Supraoptic Nucleus; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Blood Pressure; Blood Volume; Carotid Sinus; Dogs; Heart Atria; Hemorrhage; Humans; Ligation; Mechanoreceptors; Pituitary Gland, Posterior; Pressoreceptors; Pulse; Rats; Secretory Rate; Sodium; Sympathetic Nervous System; Vasopressins

Topics: Acetylcholine; Acute Kidney Injury; Angiotensin II; Animals; Bradykinin; Diuretics; Dogs; Dopamine; Electric Stimulation; Epinephrine; Heart Failure; Hemorrhage; Humans; Hypotension; Isoproterenol; Kidney Cortex; Kidney Transplantation; Liver Cirrhosis; Norepinephrine; Oxytocin; Prostaglandins; Regional Blood Flow; Transplantation, Homologous; Ureter; Vasomotor System; Vasopressins; Vena Cava, Inferior; Water-Electrolyte Balance

Topics: Diverticulum, Esophageal; Hemorrhage; Humans; Hypertension, Portal; Ligation; Liver Cirrhosis; Portacaval Shunt, Surgical; Tampons, Surgical; Vasopressins

Topics: Abdomen; Abdominal Muscles; Animals; Arteries; Blood Pressure; Carbon Dioxide; Cardiac Output; Electromyography; Feedback; Hemorrhage; Muscle Contraction; Muscle Tonus; Neurons, Afferent; Partial Pressure; Pentobarbital; Phenylephrine; Positive-Pressure Respiration; Pressure; Respiration; Vagus Nerve; Vasopressins

Topics: Angiotensin II; Animals; Catecholamines; Denervation; Dogs; Feedback; Hemorrhage; Hypertension, Renal; Hypertonic Solutions; Juxtaglomerular Apparatus; Kidney; Papaverine; Potassium Chloride; Receptors, Drug; Renal Artery; Renin; Sodium Chloride; Vasopressins

Topics: Adrenal Cortex Hormones; Adult; Analgesics; Antifibrinolytic Agents; Blood Transfusion; Cardiovascular Diseases; Child; Contraceptives, Oral; Estrogens; Factor IX; Factor VIII; Gastrointestinal Diseases; Hemarthrosis; Hemophilia A; Hemophilia B; Hemorrhage; Home Nursing; Humans; Infections; Inhalation; Nervous System Diseases; Social Adjustment; Thyroxine; Triiodothyronine; Urologic Diseases; Vasopressins

Topics: Animals; Dogs; Feedback; Hemorrhage; Mice; Vagotomy; Vasopressins

In a double-blind randomised trial, the effect of paracervical injection of vasopressin was compared with placebo on blood loss from dilatation and evacuation abortion. Vasopressin reduced blood loss significantly, an effect that became clinically more important with advancing gestational age. Blood pressure was unchanged.

Topics: Abortion, Induced; Adolescent; Adult; Blood Pressure; Clinical Trials as Topic; Dilatation and Curettage; Female; Gestational Age; Hemorrhage; Humans; Intraoperative Complications; Pregnancy; Pregnancy Trimester, Second; Random Allocation; Vasopressins

A simple technique to inject the synthetic vasoconstrictor agent ornithine-8-vasopressin endoscopically into the prostate has been developed. The method has been assessed by two prospective randomised controlled trials on patients undergoing transurethral resection of the prostate. Results from the first trial, involving 56 patients who had general anaesthesia, were that the mean operative blood loss was 48% less in the treated group, a significant difference (P = 0.05). Results from the second trial, involving 57 patients who had spinal anaesthesia, were that the mean operative blood loss was 75% less in the treated group, a highly significant difference (P = 0.01). The pharmacology of the drug is reviewed, and it seems to be a safe agent which aids transurethral resection. It frequently causes a modest and transient elevation in blood pressure shortly after injection and, although not encountered by the author, it is possible that a more severe elevation necessitating treatment may rarely occur.

Topics: Aged; Anesthesia, General; Anesthesia, Spinal; Clinical Trials as Topic; Endoscopy; Hemorrhage; Hemostasis, Surgical; Humans; Intraoperative Complications; Male; Ornipressin; Postoperative Complications; Prospective Studies; Prostatectomy; Random Allocation; Vasopressins

In a randomized, double-blind trial, haemostatic and cardiovascular effects of ornipressin and adrenaline were compared in 30 children requiring surgery for "bat-ear" deformity. Mean total blood loss was 14.3 ml with ornipressin and 11.7 ml with adrenaline, this difference being insignificant. There was a significant and progressive reduction in mean heart rate in children who received ornipressin, from 134 to 116 bpm (P less than 0.05), and a significant rise from 127 to 134 bpm (P less than 0.05) with adrenaline. Mean systolic pressure was unaltered by ornipressin but was significantly increased from 97 to 105 mmHg (P less than 0.05) in children receiving adrenaline. Ornipressin is as effective a haemostatic agent as adrenaline and the rises in heart rate and systolic pressure associated with adrenaline, which are factors known to predispose to the onset of ventricular dysrhythmias, do not occur with ornipressin.

Topics: Adult; Anesthesia, General; Blood Pressure; Double-Blind Method; Enflurane; Epinephrine; Female; Heart Rate; Hemodynamics; Hemorrhage; Hemostatics; Humans; Male; Ornipressin; Random Allocation; Vasopressins

Topics: Adult; Age Factors; Anesthesia; Blood Pressure; Cervix Uteri; Clinical Trials as Topic; Female; Heart Rate; Hemorrhage; Humans; Injections; Methods; Middle Aged; Postoperative Complications; Pregnancy; Sutures; Uterine Cervical Diseases; Vasopressins

Topics: Adult; Aged; Anesthesia, General; Blood Pressure; Clinical Trials as Topic; Electrocardiography; Halothane; Heart Rate; Hemorrhage; Humans; Middle Aged; Norepinephrine; Placebos; Radiography, Thoracic; Vasopressins

Our objective was to optimize a novel damage control resuscitation (DCR) cocktail composed of hydroxyethyl starch, vasopressin, and fibrinogen concentrate for the polytraumatized casualty. We hypothesized that slow intravenous infusion of the DCR cocktail in a pig polytrauma model would decrease internal hemorrhage and improve survival compared with bolus administration.. We induced polytrauma, including traumatic brain injury (TBI), femoral fracture, hemorrhagic shock, and free bleeding from aortic tear injury, in 18 farm pigs. The DCR cocktail consisted of 6% hydroxyethyl starch in Ringer's lactate solution (14mL/kg), vasopressin (0.8U/kg), and fibrinogen concentrate (100mg/kg) in a total fluid volume of 20mL/kg that was either divided in half and given as two boluses separated by 30 minutes as control or given as a continuous slow infusion over 60 minutes. Nine animals were studied per group and monitored for up to 3 hours. Outcomes included internal blood loss, survival, hemodynamics, lactate concentration, and organ blood flow obtained by colored microsphere injection.. Mean internal blood loss was significantly decreased by 11.1mL/kg with infusion compared with the bolus group (p = .038). Survival to 3 hours was 80% with infusion and 40% with bolus, which was not statistically different (Kaplan Meier log-rank test, p = .17). Overall blood pressure was increased (p < .001), and blood lactate concentration was decreased (p < .001) with infusion compared with bolus. There were no differences in organ blood flow (p > .09).. Controlled infusion of a novel DCR cocktail decreased hemorrhage and improved resuscitation in this polytrauma model compared with bolus. The rate of infusion of intravenous fluids should be considered as an important aspect of DCR.

Topics: Animals; Disease Models, Animal; Fibrinogen; Fluid Therapy; Hemodynamics; Hemorrhage; Hemostatics; Hydroxyethyl Starch Derivatives; Infusions, Intravenous; Isotonic Solutions; Lactates; Multiple Trauma; Resuscitation; Shock, Hemorrhagic; Swine; Vasopressins

Perioperative hyponatremia, due to non-osmotic release of the antidiuretic hormone arginine vasopressin, is a serious electrolyte disorder observed in connection with many types of surgery. Since blood loss during surgery contributes to the pathogenesis of hyponatremia, we explored the effect of bleeding on plasma sodium using a controlled hypotensive hemorrhage pig model. After 30-min baseline period, hemorrhage was induced by aspiration of blood during 30 min at mean arterial pressure <50 mmHg. Thereafter, the animals were resuscitated with retransfused blood and a near-isotonic balanced crystalloid solution and monitored for 180 min. Electrolyte and water balances, cardiovascular response, renal hemodynamics, and markers of volume regulation and osmoregulation were investigated. All pigs (n = 10) developed hyponatremia. All animals retained hypotonic fluid, and none could excrete net-free water. Urinary excretion of aquaporin 2, a surrogate marker of collecting duct responsiveness to antidiuretic hormone, was significantly reduced at the end of the study, whereas lysine vasopressin, i.e., the pig antidiuretic hormone remained high. In this animal model, hyponatremia developed due to net positive fluid balance and generation of electrolyte-free water by the kidneys. A decreased urinary aquaporin 2 excretion may indicate an escape from antidiuresis.

Topics: Animals; Aquaporin 2; Electrolytes; Hemorrhage; Hyponatremia; Sodium; Swine; Vasopressins; Water

Angiotensin II (AngII) immunoreactive cells, fibers and receptors, were found in the parvocelluar region of paraventricular nucleus (PVNp) and AngII receptors are present on vasopressinergic neurons. However, the mechanism by which vasopressin (AVP) and AngII may interact to regulate arterial pressure is not known. Thus, we tested the cardiovascular effects of blockade of the AngII receptors on AVP neurons and blockade of vasopressin V1a receptors on AngII neurons. We also explored whether the PVNp vasopressin plays a regulatory role during hypotension in anesthetized rat or not. Hypovolemic-hypotension was induced by gradual bleeding from femoral venous catheter. Either AngII or AVP injected into the PVNp produced pressor and tachycardia responses. The responses to AngII were blocked by V1a receptor antagonist. The responses to AVP were partially attenuated by AT1 antagonist and greatly attenuated by AT2 antagonist. Hemorrhage augmented the pressor response to AVP, indicating that during hemorrhage, sensitivity of PVNp to vasopressin was increased. By hemorrhagic-hypotension and bilateral blockade of V1a receptors of the PVNp, we found that vasopressinergic neurons of the PVNp regulate arterial pressure towards normal during hypotension. Taken together these findings and our previous findings about angII (Khanmoradi and Nasimi, 2017a) for the first time, we found that a mutual cooperative system of angiotensinergic and vasopressinergic neurons in the PVNp is a major regulatory controller of the cardiovascular system during hypotension.

Topics: Angiotensin I; Angiotensin II; Angiotensin II Type 2 Receptor Blockers; Animals; Arterial Pressure; Hemorrhage; Hypotension; Hypovolemia; Male; Nerve Net; Paraventricular Hypothalamic Nucleus; Rats; Rats, Sprague-Dawley; Vasopressins

Vasoactives such as terlipressin, somatostatin, vasopressin, octreotide and nitrates are commonly used to treat variceal bleeding. The present study is a network meta-analysis comparing the efficacy and safety of the above vasoactive agents for treating variceal bleeding.. Electronic databases were searched for appropriate randomized clinical trials evaluating vasoactives in cirrhotic patients with variceal bleeding. Random-effects model was used to generate the pooled estimates. Mortality was the primary outcome and bleeding control, re-bleeding rate, hospital stay, blood transfusion requirements and adverse events were the secondary outcome measures.. Fifty randomized clinical trials were included of which 37 were included for the primary outcome. The overall analysis did not reveal any significant difference in the mortality risk between any of the vaso-active drugs except for terlipressin that had statistically significant benefits from direct pooled estimates. Somatostatin and terlipressin showed significant reduction in the mortality risks at 24 h. Terlipressin significantly reduced re-bleeding rate; somatostatin and vasopressin were associated with better hemostasis; and terlipressin and vasopressin significantly reduced the requirement for blood transfusion. Terlipressin, vasopressin and glyceryltrinitrate/vasopressin were also associated with increased risk of adverse events.. Terlipressin could be the best agent in the vasoconstrictor category for managing variceal bleeding. Somatostatin and vasopressin can serve as alternatives.

Topics: Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Hemorrhage; Humans; Network Meta-Analysis; Octreotide; Randomized Controlled Trials as Topic; Somatostatin; Terlipressin; Vasoconstrictor Agents; Vasopressins

Hypothermia preserves gastric mucosal microvascular oxygenation (μHbO2) during hemorrhagic shock. Additionally, hypothermia activates the sympathetic nervous system that leads to the release of vasopressin. The aim of this study was to evaluate whether the effect of hypothermia is mediated via the sympathetic nervous system and/or via vasopressin.. In prospective and randomized experiments on five anesthetized dogs (foxhounds, cross-over design, 6 groups with n=5 per group) we analyzed the effects of hemorrhage on μHbO2 during mild hypothermia (HT, 34 °C), during additional thoracic epidural anesthesia (HT/TEA) and during additional vasopressin V1 receptor blockade (HT/VB). As control groups, effects of hemorrhage were studied under normothermia alone (NT), during additional thoracic epidural anesthesia (NT/TEA) and during additional vasopressin V1 receptor blockade (NT/VB).. Hemorrhage decreased μHbO2 from 81 ± 3 to 49 ± 8%. In contrast, in the presence of hypothermia, μHbO2 was significantly higher during hemorrhagic shock (from 79 ± 3 to 66 ± 9%) despite a similar decrease in DO2. The effect of hypothermia on μHbO2 was reduced in the presence of thoracic epidural anesthesia or vasopressin receptor blockade.. Hypothermia preserves μHbO2 during hemorrhagic shock. This effect is partially abolished during thoracic epidural anesthesia or during vasopressin receptor blockade. The sympathetic nervous system and the vasopressin V1 receptor are partially involved in mediating the effect of hypothermia on gastric oxygenation during hemorrhage.

Topics: Anesthesia, Epidural; Animals; Antidiuretic Hormone Receptor Antagonists; Arginine Vasopressin; Dogs; Female; Gastric Mucosa; Hemorrhage; Hypothermia; Lidocaine; Oxygen; Sympathetic Nervous System; Vasopressins

This study investigated the cardiovascular effects of nesfatin-1 in normotensive rats and animals subjected to hypotensive hemorrhage. Hemorrhagic hypotension was induced by withdrawal 2 mL blood/100 g body weight over a period of 10 min. Acute hemorrhage led to a severe and long-lasting decrease in mean arterial pressure (MAP) and heart rate (HR). Intracerebroventricularly (i.c.v.) administered nesfatin-1 (100 pmol) increased MAP in both normotensive and hemorrhaged rats. Nesfatin-1 also caused bradycardia in normotensive and tachycardia in hemorrhaged rats. Centrally injected nesfatin-1 (100 pmol, i.c.v.) also increased plasma catecholamine, vasopressin and renin concentrations in control animals and potentiated the rise in all three cardiovascular mediators produced by hemorrhage. These findings indicate that centrally administered nesfatin-1 causes a pressor response in conscious normotensive and hemorrhaged rats and suggest that enhanced sympathetic activity and elevated vasopressin and renin concentrations mediate the cardiovascular effects of the peptide.

Topics: Animals; Blood Pressure; Bradycardia; Calcium-Binding Proteins; Catecholamines; Central Nervous System Agents; Disease Models, Animal; DNA-Binding Proteins; Heart Rate; Hemorrhage; Hypotension; Male; Nerve Tissue Proteins; Nucleobindins; Rats, Sprague-Dawley; Renin; Vasopressins

Adrenaline (ADR) and vasopressin (VAS) are used as vasopressors during cardiopulmonary resuscitation. Data regarding their effects on blood-brain barrier (BBB) integrity and neuronal damage are lacking. We hypothesised that VAS given during cardiopulmonary resuscitation (CPR) after haemorrhagic circulatory arrest will preserve BBB integrity better than ADR.. Twenty-one anaesthetised sexually immature male piglets (with a weight of 24.3 ± 1.3 kg) were bled 35% via femoral artery to a mean arterial blood pressure of 25 mmHg in the period of 15 min. Afterwards, the piglets were subjected to 8 min of untreated ventricular fibrillation followed by 15 min of open-chest CPR. At 9 min of circulatory arrest, piglets received amiodarone 1.0 mg/kg and hypertonic-hyperoncotic solution 4 ml/kg infusions for 20 min. At the same time, VAS 0.4 U/kg was given intravenously to the VAS group (n = 9) while the ADR group received ADR 20 μg/kg (n = 12). Internal defibrillation was attempted from 11 min of cardiac arrest to achieve restoration of spontaneous circulation. The experiment was terminated 3 h after resuscitation.. The intracranial pressure (ICP) in the post-resuscitation phase was significantly greater in ADR group than in VAS group. VAS group piglets exhibited a significantly smaller BBB disruption compared with ADR group. Cerebral pressure reactivity index showed that cerebral blood flow autoregulation was also better preserved in VAS group.. Resuscitation with ADR as compared with VAS after haemorrhagic circulatory arrest increased the ICP and impaired cerebrovascular autoregulation more profoundly, as well as exerted an increased BBB disruption though no significant difference in neuronal injury was observed.

Topics: Amiodarone; Animals; Blood-Brain Barrier; Capillary Permeability; Cardiopulmonary Resuscitation; Cerebrovascular Circulation; Dobutamine; Electric Countershock; Enzyme Activation; Epinephrine; Fluid Therapy; Heart Arrest; Hemodynamics; Hemorrhage; Intracranial Pressure; Male; Nitric Oxide Synthase Type I; Nitric Oxide Synthase Type II; Sus scrofa; Swine; Vasopressins; Ventricular Fibrillation

Supplemental digital content is available in the text.. The aim of this experimental study was to compare survival and hemodynamic effects of a low-dose amiodarone and vasopressin compared with vasopressin in hypovolemic cardiac arrest model in piglets.. Eighteen anesthetized male piglets (with a weight of 25.3 [1.8] kg) were bled approximately 30% of the total blood volume via the femoral artery to a mean arterial blood pressure of 35 mm Hg in a 15-minute period. Afterward, the piglets were subjected to 4 minutes of untreated ventricular fibrillation followed by 11 minutes of open-chest cardiopulmonary resuscitation. At 5 minutes, circulatory arrest amiodarone 1 mg/kg was intravenously administered in the amiodarone group (n = 9), while the control group received the same amount of saline (n = 9). At the same time, all piglets received vasopressin 0.4 U/kg intravenously administered and hypertonic-hyperoncotic solution 3-mL/kg infusion for 20 minutes. Internal defibrillation was attempted from 7 minutes of cardiac arrest to achieve restoration of spontaneous circulation. The experiment was terminated 3 hours after resuscitation.. Three-hour survival was greater in the amiodarone group (p = 0.02). After the successful resuscitation, the amiodarone group piglets had significantly lower heart rate as well as greater systolic, diastolic, and mean arterial pressure. Troponin I plasma concentrations were lower and urine output was greater in the amiodarone group.. Combined resuscitation with amiodarone and vasopressin after hemorrhagic circulatory arrest resulted in greater 3-hour survival, better preserved hemodynamic parameters, and smaller myocardial injury compared with resuscitation with vasopressin only.

Topics: Amiodarone; Animals; Antidiuretic Agents; Disease Models, Animal; Dose-Response Relationship, Drug; Drug Therapy, Combination; Heart Arrest; Hemodynamics; Hemorrhage; Injections, Intravenous; Male; Resuscitation; Swine; Treatment Outcome; Vasodilator Agents; Vasopressins; Ventricular Fibrillation

To test the compensatory role of endothelin-1 when acute blood loss is superimposed on anaesthesia, by characterizing the effect of systemic endothelin receptor subtype A (ET(A)) blockade on the haemodynamic and hormonal responses to haemorrhage in dogs anaesthetized with xenon/remifentanil (X/R) or isoflurane/remifentanil (I/R).. Prospective experimental randomized controlled study.. Six female Beagle dogs, 13.4 +/- 1.3 kg.. Animals were anaesthetized with remifentanil 0.5 microg kg(-1) minute(-1) plus either 0.8% isoflurane (I/R) or 63% xenon (X/R), with and without (Control) the systemic intravenous endothelin receptor subtype A antagonist atrasentan (four groups, n = 6 each). After 60 minutes of baseline anaesthesia, the dogs were bled (20 mL kg(-1)) over 5 minutes and hypovolemia was maintained for 1 hour. Continuous haemodynamic monitoring was performed via femoral and pulmonary artery catheters; vasoactive hormones were measured before and after haemorrhage.. In Controls, systemic vascular resistance (SVR), vasopressin and catecholamine plasma concentrations were higher with X/R than with I/R anaesthesia at pre-haemorrhage baseline. The peak increase after haemorrhage was higher during X/R than during I/R anaesthesia (SVR 7420 +/- 867 versus 5423 +/- 547 dyne seconds cm(-5); vasopressin 104 +/- 23 versus 44 +/- 6 pg mL(-1); epinephrine 2956 +/- 310 versus 177 +/- 99 pg mL(-1); norepinephrine 862 +/- 117 versus 195 +/- 33 pg mL(-1), p < 0.05). Haemorrhage reduced central venous pressure from 3 +/- 1 to 1 +/- 1 cm H(2)O (I/R, ns) and from 8 +/- 1 to 5 +/- 1 cm H(2)O (X/R, p < 0.05), but did not reduce mean arterial pressure, nor cardiac output. Atrasentan did not alter the haemodynamic and hormonal response to haemorrhage during either anaesthetic protocol.. Selective ET(A) receptor blockade with atrasentan did not impair the haemodynamic and hormonal compensation of acute haemorrhage during X/R or I/R anaesthesia in dogs.

Topics: Anesthesia; Anesthesia, Inhalation; Anesthesia, Intravenous; Anesthetics, Inhalation; Anesthetics, Intravenous; Animals; Atrasentan; Blood Loss, Surgical; Catecholamines; Dog Diseases; Dogs; Endothelin A Receptor Antagonists; Endothelin-1; Epinephrine; Female; Hemodynamics; Hemorrhage; Isoflurane; Norepinephrine; Piperidines; Pyrrolidines; Remifentanil; Time Factors; Vascular Resistance; Vasopressins; Xenon

1. The aims of the present study were to determine the cardiovascular effects of arachidonic acid (AA) and to investigate the peripheral mechanisms mediating these effects in haemorrhage-induced hypotensive rats. 2. Acute haemorrhage was induced by withdrawing a total volume of 2.2 mL blood/100 g bodyweight over a period of 10 min. Rats were then injected with 75-300 microg, i.c.v., AA and cardiovascular changes were monitored over the next 60 min. Plasma catecholamine and vasopressin levels, as well as plasma renin activity (PRA), were measured 10 min after injection of 150 microg AA in haemorrhage-induced hypotensive awake rats. In addition, rats were pretreated with saline (1 mL/kg, i.v.), the vasopressin V(1) receptor antagonist [beta-mercapto-beta,beta-cyclopentamethylenepropionyl(1),O-Me-Tyr(2),Arg(8)]-vasopressin (10 microg/kg, i.v.), the alpha(1)-adrenoceptor antagonist prazosin (500 microg/kg, i.v.), the non-specific angiotensin II receptor antagonist saralasin (250 microg/kg, i.v.) or a combination of these three antagonists 5 min before injection of AA (150 microg, i.c.v.). The effects of these antagonists on responses to AA were determined. 3. Arachidonic acid caused dose- and time-dependent increases in mean arterial pressure and heart rate and reversed hypotension in haemorrhaged rats. Haemorrhage itself produced an increase in plasma catecholamine and vasopressin levels, as well as PRA; injection of AA produced further increases in these parameters, ranging from 39-123%, under hypotensive conditions. Under hypotensive conditions, pretreatment of rats with all three receptor antagonists produced similar partial blockade of the pressor response to AA, but not the increase in heart rate. Moreover, combined administration of all three receptor antagonists prior to the i.c.v. injection of 150 microg AA completely abolished the pressor response to AA in haemorrhage-induced hypotensive rats. 4. These results indicate that centrally administered AA reverses hypotension by increasing blood pressure and heart rate in the hypotensive setting. The observed increases in plasma catecholamine and vasopressin levels, as well as PRA, mediate the pressor response to AA in haemorrhage-induced hypotensive rats.

Topics: Adrenergic alpha-1 Receptor Antagonists; Angiotensin Receptor Antagonists; Animals; Antidiuretic Hormone Receptor Antagonists; Arachidonic Acid; Blood Pressure; Cardiovascular System; Catecholamines; Consciousness; Drug Evaluation, Preclinical; Heart Rate; Hemorrhage; Hormone Antagonists; Hypotension; Injections, Intraventricular; Male; Rats; Rats, Sprague-Dawley; Signal Transduction; Vasopressins

The effects of endothelin receptor subtype A (ETA) blockade on hemodynamics and hormonal adaptation during hemorrhage were studied in xenon/remifentanil-anesthetized dogs (n=6) pretreated with an angiotensin II type 1 (AT1)-receptor blocker.. after a baseline awake period, anesthesia was induced in the dogs with propofol and maintained with xenon/remifentanil (baseline anesthesia). Sixty minutes later, 20 mL x kg(-1) of blood was withdrawn within 5 min and the dogs observed for another hour (hemorrhage). AT1 group followed the same protocol as controls except the AT1-receptor blocker losartan (i.v. 100 microg x kg(-1) x min(-1)) was started at the beginning of the experiment. AT1+ETA group was the same as AT1 group but with the addition of the ETA-receptor blocker atrasentan (i.v. 1 mg x kg(-1), then 0.01 mg x kg(-1) x min(-1)). In controls, mean arterial pressure (MAP) remained unchanged during baseline anesthesia, whereas systemic vascular resistance (SVR) increased from 3282+/-281 to 7321+/-803 dyn.s.cm-5, heart rate (HR) decreased from 86+/-4 to 40+/-3 beats x min(-1), and cardiac output (CO) decreased from 2.3+/-0.2 to 0.9+/-0.1 L x min(-1) (p<0.05), with no further changes after hemorrhage. In AT1-inhibited dogs, MAP (71+/-6 mm Hg) and SVR (5939+/-611 dyn x s x cm(-5)) were lower during baseline anesthesia and after hemorrhage, but greater than those in AT1+ETA (66+/-7 mm Hg, 5034+/-658 dyn x s x cm(-5)) (p<0.05). HR and CO were not different between groups. Plasma concentration of vasopressin was highest with AT1+ETA inhibition after hemorrhage. Combined AT1+ETA-receptor blockade impaired vasoconstriction more than did AT1-receptor blockade alone, both during baseline xenon anesthesia and after hemorrhage. Even a large increase in vasoconstrictor hormones could not prevent the decrease in blood pressure and the smaller increase in SVR. Thus, endothelin is an important vasoconstrictor during hemorrhage, and both endothelin and angiotensin II are essential hormones for cardiovascular stabilization after hemorrhage.

Topics: Anesthesia; Angiotensin II; Angiotensin II Type 1 Receptor Blockers; Animals; Atrasentan; Blood Pressure; Dogs; Endothelin A Receptor Antagonists; Endothelin-1; Female; Hemodynamics; Hemorrhage; Losartan; Pyrrolidines; Vascular Resistance; Vasoconstriction; Vasopressins; Xenon

Central administration of choline increases blood pressure in normotensive and hypotensive states by increasing plasma concentrations of vasopressin and catecholamines. We hypothesized that choline could also modulate the renin-angiotensin pathway, the third main pressor system in the body. Plasma renin activity (PRA), which serves as an index of the function of the peripheral renin-angiotensin system, was determined in rats subjected to graded haemorrhage following central choline administration. Intracerebroventricular (i.c.v.) injection of choline (12.5-150 microg), a precursor of the neurotransmitter acetylcholine (ACh), inhibited the increase in PRA in rats subjected to graded haemorrhage by sequential removal of 0.55 mL blood/100 g bodyweight. Choline, in the range 50-150 microg, increased blood pressure. Intraperitoneal (i.p.) administration of 150 microg choline failed to alter blood pressure and plasma renin responses to graded haemorrhage. Administration of a higher dose (90 mg/kg, i.p.) of choline decreased blood pressure and enhanced PRA in the first two blood samples obtained during the graded haemorrhage. Physostigmine (10 microg, i.c.v.), ACh (10 microg, i.c.v.), carbamylcholine (10 microg, i.c.v.) and cytidine 5'-diphosphocholine (CDP-choline; 250 microg, i.c.v.) increased blood pressure and attenuated plasma renin responses to graded haemorrhage. Inhibition of PRA by i.c.v. choline was abolished by i.c.v. pretreatment with mecamylamine (50 microg), but not atropine (10 microg). Blood pressure responses to choline (150 microg) were attenuated by pretreatment with both mecamylamine and atropine. Inhibition of PRA in response to central choline administration was associated with enhanced plasma vasopressin and catecholamine responses to graded haemorrhage. Pretreatment of rats with a vasopressin antagonist reversed central choline-induced inhibition of plasma renin responses to graded haemorrhage without altering the blood pressure response. In conclusion, central administration of choline inhibits the plasma renin response to graded haemorrhage. Nicotinic receptor activation and an increase in plasma vasopressin appear to be involved in this effect.

Topics: Animals; Antihypertensive Agents; Blood Pressure; Carbachol; Choline; Cholinergic Agonists; Cholinesterase Inhibitors; Cytidine Diphosphate Choline; Dose-Response Relationship, Drug; Drug Interactions; Female; Hemorrhage; Injections, Intraventricular; Mecamylamine; Periodicity; Physostigmine; Rats; Rats, Wistar; Renin; Renin-Angiotensin System; Vasopressins

In Wistar rats, an increase in renal sympathetic activity is induced by activation of presympathetic neurones in the paraventricular nucleus (PVN) and reflexly by a mild venous haemorrhage. Both stimuli are dependent on the release of vasopressin and glutamate at spinal synapses. The significance of the supraspinal pathway and the co-operative interaction of vasopressin with an excitatory amino acid is unclear. The present study examines this in Brattleboro rats, which have a natural vasopressin gene deletion. The responses were compared with Long-Evans rats, from which Brattleboro rats are derived. All rats were anaesthetized with a mixture of urethane (650 mg kg(-1) i.v.) and chloralose (50 mg kg(-1) i.v.). Recordings were made of blood pressure, heart rate and renal sympathetic nerve activity (RSNA). Microinjection of d,l-homocysteic acid (DLH, 0.2 m, 100 nl) at sites restricted to the PVN elicited significant increases in RSNA (P < 0.001) in both strains of rats. These changes were significantly reduced (P < 0.01) in Long-Evans rats by intrathecal application to the spinal cord of either a V(1a) antagonist or a glutamate antagonist (kynurenic acid), whereas in Brattleboro rats the changes were significantly reduced (P < 0.05) only by kynurenic acid. Removal of 1 ml of venous blood in Long-Evans rats increased RSNA by 28 +/- 4% (P < 0.01), which was significantly reduced (P < 0.05) by prior intrathecal application of either the V(1a) antagonist or by kynurenic acid. The same test in Brattleboro rats caused a significantly greater (P < 0.05) increase (63 +/- 14.7%) in RSNA which, in contrast to Long-Evans rats, was unchanged by intrathecal application of the V(1a) antagonist, being significantly reduced (P < 0.01) only by intrathecal kynurenic acid. Thus, in Brattleboro rats, the lack of vasopressin in the brain sympathetic pathways appears to be compensated, acutely, by glutamate-releasing pathways. This might indicate that, in normal rats, vasopressin is more important in maintaining longer term adjustments to stressors.

Topics: Animals; Blood Pressure; Excitatory Amino Acid Antagonists; Glutamic Acid; Heart Rate; Hemorrhage; Homocysteine; Kidney; Kynurenic Acid; Male; Neurons; Paraventricular Hypothalamic Nucleus; Rats; Rats, Brattleboro; Rats, Long-Evans; Spinal Nerves; Sympathetic Nervous System; Vasopressins

Acute NaCl loading as resuscitation in haemorrhagic hypovolaemia is known to induce rapid cardiovascular recovery. Besides an osmotically induced increase in plasma volume the physiological mechanisms of action are unknown. We hypothesized that a CNS mechanism, elicited by increased periventricular [Na(+)] and mediated by angiotensin II type 1 receptors (AT(1)), is obligatory for the full effect of hypertonic NaCl. To test this we investigated the cardiovascular responses to haemorrhage and subsequent hypertonic NaCl infusion (7.5% NaCl, 4 ml (kg BW)(-1)) in six conscious sheep subjected to intracerebroventricular (i.c.v.) infusion of artificial cerebrospinal fluid (aCSF; control), mannitol solution (Man; 75 mmol l(-1) [Na(+)], total osmolality 295 mosmol kg(-1)) or losartan (Los; 1 mg ml(-1), AT(1) receptor antagonist) at three different occasions. Man normalized (144 +/- 6 mmol l(-1), mean +/- s.d.) the increase in i.c.v. [Na(+)] seen after aCSF (161 +/- 2 mmol l(-1)). Compared with control, both Man and Los significantly (P < 0.05) attenuated the improvement in mean arterial blood pressure (MAP), cardiac index and mesenteric blood flow (SMBF) in response to intravenous hypertonic NaCl: MAP, rapid response +45 mmHg versus +38 mmHg (Man) and +35 mmHg (Los); after 180 min, +32 mmHg versus +21 mmHg (Man) and +19 mmHg (Los); cardiac index after 180 min, +1.9 l min(-1) (m(2))(-1) versus +0.9 l min(-1) (m(2))(-1) (Man) and +0.9 l min(-1) (m(2))(-1) (Los); SMBF rapid response, +981 ml min(-1) versus +719 ml min(-1) (Man) and +744 ml min(-1) (Los); after 180 min, +602 ml min(-1) versus +372 ml min(-1) (Man) and +314 ml min(-1) (Los). The results suggest that increased periventricular [Na(+)] and cerebral AT(1) receptors contribute, together with plasma volume expansion, to improve systemic haemodynamics after treatment with hypertonic NaCl in haemorrhagic hypovolaemia.

Topics: Angiotensin II; Angiotensin II Type 1 Receptor Blockers; Animals; Blood Pressure; Cardiovascular System; Consciousness; Diuretics, Osmotic; Female; Hemorrhage; Hypovolemia; Infusions, Intravenous; Injections, Intraventricular; Losartan; Mannitol; Osmolar Concentration; Receptor, Angiotensin, Type 1; Resuscitation; Saline Solution, Hypertonic; Sheep; Sodium; Vascular Resistance; Vasopressins

We have previously shown that centrally injected melittin, a phospholipase A(2) (PLA(2)) activator, increases blood pressure and decreases heart rate in the normotensive conscious rats. In the current study we aimed to determine the cardiovascular effects of melittin in hemorrhaged hypotensive rats and to investigate the mediation of peripheral adrenergic, vasopressinergic and renin angiotensin system in the pressor effect of centrally administrated melittin in both normotensive and hypotensive conditions. Acute hypotensive hemorrhage was performed by withdrawing a total volume of 2.2ml of blood/100g body weight over a period of 10min. Melittin was injected intracerebroventricularly (i.c.v.) at the doses of 1.5microg, 3.0microg or 6.0microg after the stabilization period of hemorrhage procedure. We also repeated previous experiments by injecting melittin (1.5microg, 3.0microg or 6.0microg; i.c.v.) to the normotensive animals. Melittin caused dose- and time-dependent increases in mean arterial pressure (MAP) in normal and hypotensive conditions and decreases in heart rate (HR) in normotensive conscious animals. In hypotensive rats, melittin injected at the dose of 6.0microg completely restored the decrease in blood pressure. Plasma adrenaline, noradrenaline, vasopressin levels and renin activity increased after melittin (3.0microg; i.c.v) administration in normal conditions. Hemorrhage, itself, produced an increase in these plasma hormone levels and melittin (3.0microg; i.c.v.) caused additional increases in plasma adrenaline, noradrenaline, vasopressin levels and renin activity in hypotensive conditions. Intravenous pretreatments of rats with prazosin (0.5mg/kg), an alpha(1) adrenoceptor antagonist, [beta-mercapto-beta,beta-cyclopentamethylenepropionyl(1), O-Me-Tyr(2)-Arg(8)]-vasopressin (10microg/kg), a vasopressin V(1) receptor antagonist, or saralasin (250microg/kg), an angiotensin II receptor antagonist, partially blocked the pressor response to melittin (3.0microg; i.c.v.) in both normotensive and hypotensive conditions. Besides, the combined administration of these three antagonists before melittin completely abolished the pressor responses to drug in both conditions. Results show that centrally administered melittin, a PLA(2) activator, increases blood pressure and reverses hypotension in hemorrhagic shock. The increases in plasma adrenaline, noradrenaline, vasopressin levels and renin activity mediate the pressor responses to melittin in normal an

Topics: Animals; Blood Pressure; Cardiovascular System; Epinephrine; Hemorrhage; Hypotension; Male; Melitten; Norepinephrine; Rats; Rats, Sprague-Dawley; Vasopressins

The present study sought to determine whether chemical destruction of peripheral catecholaminergic fibers with 6-hydroxydopamine (6OHDA) attenuates vasopressin (VP) and oxytocin (OT) secretion stimulated by hemorrhage, hypotension, and hyperosmolality. Rats received 6OHDA (100 mg/kg iv) or vehicle (1 ml/kg iv) on days 1 and 7, and experiments were performed on day 8. Serial hemorrhage (4 samples of 2 ml per 300 g body wt at 10-min intervals) increased plasma VP and OT levels in both groups; however, the increase in plasma VP and OT levels was significantly attenuated in 6OHDA-treated vs. control rats despite a significantly lower mean arterial blood pressure. Similarly, the increase in plasma VP and OT levels in response to hypotension produced by the selective arteriolar vasodilator diazoxide was significantly attenuated in 6OHDA-treated rats. In marked contrast to hemorrhage and hypotension, hyperosmolality produced by an infusion of 1 M NaCl (2 ml/h iv) stimulated increases in plasma VP and OT levels that were not different between 6OHDA-treated and control rats. In a parallel set of experiments, intravenous 6OHDA treatment reduced dopamine--hydroxylase immunoreactivity in the posterior pituitary but had no substantial effect in the hypothalamic paraventricular and supraoptic nuclei. In each experiment, the pressor response to tyramine (250 microg/kg iv) was significantly attenuated in 6OHDA-treated rats, thereby confirming that 6OHDA treatment destroyed sympathetic catecholaminergic fibers. Collectively, these findings suggest that catecholaminergic fibers located outside the blood-brain barrier contribute to VP and OT secretion during hemorrhage and arterial hypotension.

Topics: Animals; Diazoxide; Dopamine beta-Hydroxylase; Hemorrhage; Hypotension; Hypothalamus; Injections, Intravenous; Male; Oxidopamine; Oxytocin; Pituitary Gland, Posterior; Rats; Rats, Sprague-Dawley; Sympatholytics; Tyramine; Vasopressins; Water-Electrolyte Imbalance

This study investigated the importance of supraspinal vasopressin and glutamate neurones in regulating renal sympathetic activity as part of the response to an acute reduction in blood volume. Wistar rats anaesthetized with chloralose and urethane were instrumented to record arterial blood pressure, heart rate and left renal sympathetic nerve activity. Pharmacological agonists and antagonists to glutamate and vasopressin were applied to the renal outflow of the spinal cord via an intrathecal catheter inserted at the foramen magnum and with the tip at the level of T10. Both glutamate and vasopressin increased renal sympathetic activity, and these actions were shown to be selectively blocked by their respective antagonists. Removing 1 ml of venous blood from a femoral venous catheter elicited an increase of 26 +/- 2% in renal sympathetic activity. This response to mild haemorrhage was halved to 13 +/- 4% by prior intrathecal application of a selective V1a antagonist. Similarly, prior intrathecal application of kynurenic acid reduced the response to the mild haemorrhage from 28 +/- 2 to 12.6 +/- 2.8%. Intrathecal application of both antagonists together reduced the haemorrhage response even further to 8 +/- 3%. All the changes were statistically significant at P < 0.01. It is concluded that a small reduction in blood volume induces an increase in renal sympathetic activity dependent on vasopressin and glutamate release from terminals of supraspinal neurones. It is suggested that the vasopressin neurones most probably originate from the paraventricular nucleus of the hypothalamus.

Topics: Adaptation, Physiological; Animals; Glutamic Acid; Hemorrhage; Kidney; Male; Neurons; Rats; Rats, Wistar; Spinal Cord; Sympathetic Nervous System; Vasopressins

The endogenous corticotropin-releasing factor (CRF) type 2 receptor (CRFR2)-selective ligand urocortin 3 is expressed in discrete subcortical brain regions with fibers distributed mainly to hypothalamic and limbic structures. Close anatomical association between major urocortin 3 terminal fields and CRFR2 in hypothalamus, lateral septum, and medial amygdala (MEA) suggest it is well placed to modulate behavioral and hormonal responses to stress. Urocortin 3 was administered intracerebroventricularly to male rats under basal conditions or before a restraint stress, and circulating ACTH, corticosterone, glucose, and insulin were measured. Urocortin 3 activated the hypothalamic-pituitary-adrenal axis under basal conditions and augmented ACTH responses to restraint stress. Elevated blood glucose with lowered insulin to glucose ratios in both groups suggested increased sympathetic activity. Circulating catecholamines were also increased by urocortin 3, providing additional evidence for sympathoadrenomedullary stimulation. Intracerebroventricular urocortin 3 increased vasopressin mRNA expression in the parvocellular division of the hypothalamic paraventricular nucleus, whereas CRF expression was unchanged, providing a possible mechanism by which urocortin 3 mediates its actions. Urocortin 3 mRNA expression was examined after exposure to stress-related paradigms. Restraint increased levels in MEA with a trend to increased expression in the rostral perifornical hypothalamic area, whereas hemorrhage and food deprivation decreased expression in MEA. Adrenalectomy markedly increased expression in the rostral perifornical hypothalamic area, and high-level corticosterone replacement restored this to control levels. The evidence that urocortin 3 has the potential to influence hormonal components of the stress response and the changes in its expression levels after stressors is consistent with a potential function for the endogenous peptide in modulating stress responses.

Topics: Adrenalectomy; Amygdala; Animals; Blood Glucose; Catecholamines; Corticotropin-Releasing Hormone; Food Deprivation; Glucocorticoids; Hemorrhage; Hypothalamus; In Situ Hybridization; Injections, Intravenous; Injections, Intraventricular; Male; Neurosecretory Systems; Rats; Rats, Sprague-Dawley; Restraint, Physical; RNA, Messenger; Stress, Psychological; Urocortins; Vasopressins

We report the successful use of a low-dose vasopressin (VP) infusion to recover a hypotensive crisis in patients who suffered persistent hypotension after prolonged hemorrhage during general anesthesia. VP was infused in two posthemorrhagic vasodilatory shock patients when they remained persistently hypotensive despite adequate fluid resuscitation and infusions of pharmacological doses of catecholamines. On administration of VP at 0.04 U x min(-1), systemic vascular resistance, systolic arterial pressure, and urine output were immediately increased (as compared with the values obtained just before VP), and infusion of catecholamine could be decreased. No adverse cardiac effects were observed during VP infusions in these patients. During vasodilatory shock after prolonged and severe hemorrhage, VP seems to be effective in reversing hypotension and decreasing the need for exogenous cathecholamines while preserving cardiac function and critical organ blood flow.

Topics: Anesthesia, General; Hemorrhage; Humans; Hypotension; Male; Middle Aged; Vasodilation; Vasopressins

This study aimed to investigate the roles of glutamate (Glu) receptors in the anteroventral third ventricular region (AV3V), a pivotal area for water, cardiovascular and neuroendocrine regulations, in causing vasopressin (AVP) secretion and other phenomena in response to bleeding. The effects of intracerebral infusions of MK-801 [a N-methyl-D-aspartate (NMDA) receptor antagonist] or a metabotropic Glu receptor antagonist (MCPG) on plasma levels of AVP, electrolytes, osmolality and glucose, heart rate and arterial pressure following AV3V administration with NMDA or bleeding stimuli were analyzed in conscious rats. NMDA provoked prominent rises of plasma AVP, osmolality, glucose and arterial pressure, without changing plasma electrolytes or heart rate significantly. All the effects of NMDA were blocked by pre-administration of MK-801 into the same loci. Removal through a femoral arterial line of 10 ml blood per kg body weight did not affect arterial pressure or other variables significantly, although plasma AVP and angiotensin II (ANG II) tended to increase. When bleeding was repeated after 10 min (B2), arterial pressure dropped promptly, and plasma AVP, ANG II, osmolality and glucose augmented remarkably. MK-801 applied 35 min preceding B2, to loci such as the median preoptic nucleus, periventricular nucleus and medial preoptic area inhibited the response of plasma AVP significantly, without exerting any effects on other variables. When MK-801 was administered intracerebroventricularly, or when MCPG was infused into the AV3V, significant alterations did not occur in B2-evoked responses of plasma AVP nor in those of the other variables. In rats given sham bleeding after AV3V infusions of MK-801 or MCPG or intracerebroventricular applications of MK-801, all monitored variables roughly remained at stable levels throughout the experiments. We conclude that NMDA receptors in AV3V, but not metabotropic Glu receptors, may facilitate AVP secretion in hypotensive hypovolemia.

Topics: Analysis of Variance; Angiotensin II; Animals; Blood Glucose; Blood Pressure; Dizocilpine Maleate; Drug Interactions; Electrolytes; Excitatory Amino Acid Antagonists; Glycine; Heart Rate; Hemorrhage; Hypothalamus; Injections, Intraventricular; Male; N-Methylaspartate; Osmolar Concentration; Rats; Rats, Wistar; Receptors, Metabotropic Glutamate; Receptors, N-Methyl-D-Aspartate; Third Ventricle; Time Factors; Vasopressins; Wakefulness

Topics: Catecholamines; Diaphragm; Hemorrhage; Humans; Perfusion; Regional Blood Flow; Shock, Hemorrhagic; Vasoconstrictor Agents; Vasopressins; Wounds and Injuries

1. In the present study, we aimed to determine the involvement of brain thromboxane A2 (TXA2) in blood pressure decreases evoked by acute and/or graded haemorrhage in rats. 2. Sprague-Dawley rats were used throughout the study. Acute haemorrhage was achieved by withdrawing a total volume of 2.1 and 2.5 mL blood/100 g bodyweight over a period of 10 min. A microdialysis study was performed in a hypothalamic area to measure extracellular TXA2 levels. Graded haemorrhage was conducted successively by withdrawing carotid arterial blood (0.55 mL/100 g bodyweight) over a 10 s period four times (S1-S4) at 5 min intervals. Furegrelate (125, 250 and 500 microg), a TXA2 synthase inhibitor, was injected intracerebroventricularly (i.c.v.) 60 min before acute or graded haemorrhage was initiated. U-46619 (0.5, 1 and 2 microg, i.c.v.), a synthetic TXA2 analogue, was administered 5 min before acute haemorrhage (2.1 mL/100 g bodyweight). 3. Acute haemorrhage produced a severe and long-lasting decrease in blood pressure and had a tendency to increase heart rate. Both haemorrhage protocols (2.1 or 2.5 mL/100 g) generated similar approximate twofold increases in extracellular hypothalamic TXA2 levels. Intracerebroventricular furegrelate (250 microg) pretreatment completely blocked the TXA2 increases induced by acute haemorrhage. Furegrelate administration (100, 250 and 500 microg, i.c.v.) attenuated the fall in arterial pressure evoked by acute haemorrhage and caused significant increases in heart rate at all doses injected. 4. Graded haemorrhage progressively lowered arterial pressure and increased plasma vasopressin and adrenaline levels in the last period. Furegrelate-injected rats were greatly resistant to the hypotensive effect of haemorrhage for all degrees of blood removed. Plasma adrenaline and vasopressin levels were significantly elevated in furegrelate-pretreated rats compared with the saline-treated group during S2-S3 and S4, respectively. U-46619 administration caused small but statistically significant decreases in arterial pressure induced by haemorrhage. 4. The results show that acute hypotensive haemorrhage increases extracellular hypothalamic TXA2 levels. The increase in brain endogenous TXA2 levels involves a decrease in blood pressure evoked by haemorrhage because the blockade of TXA2 synthesis by furegrelate pretreatment attenuated the haemorrhagic hypotension. Increases in plasma adrenaline and vasopressin levels may mediate this effect.

Topics: 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; Animals; Benzofurans; Blood Pressure; Disease Models, Animal; Epinephrine; Heart Rate; Hemorrhage; Hypotension; Hypothalamus; Injections, Intraventricular; Male; Rats; Rats, Sprague-Dawley; Thromboxane A2; Thromboxane-A Synthase; Time Factors; Vasoconstrictor Agents; Vasopressins

In the present study, we investigated the cardiovascular effects of centrally injected U-46619, a thromboxane A(2) (TXA(2)) analog, and the central and peripheral mechanisms of these effects in hemorrhagic shock conditions. Hemorrhage was performed by withdrawing a total volume of 2.1 ml of blood/100 g body weight over a period of 10 min. Injections were made into the lateral cerebral ventricle (LCV), nucleus tractus solitarius (NTS), rostral ventrolateral medulla (RVLM) and paraventricular nucleus of hypothalamus (PVN). U-46619 (0.1, 1 and 2 microg) increased blood pressure and reversed hypotension in hemorrhagic shock. The pressor effect was dose- and time-dependent in all investigated brain areas. Heart rate changes were not significantly different in all groups. Pretreatment of rats with an injection of SQ-29548 (4 or 8 microg), a TXA(2) receptor antagonist, into the LCV, NTS, RVLM and PVN completely blocked the pressor effect of U-46619 (1 microg) injected into respective brain areas. Hemorrhage itself increased plasma adrenaline, noradrenaline, vasopressIN levels and renin activity. U-46619 (1 microg) injected into the LCV, PVN, RVLM and NTS produced additional increases in these hormone levels and in renin activity. Intravenous pretreatments of rats with prazosin (0.5 mg/kg), an alpha(1)-adrenoceptor antagonist, [beta-mercapto-beta,beta-cyclopentamethylenepropionyl(1), O-Me-Tyr(2),Arg(8)]- vasopressin (10 microg/kg), a vasopressin V(1)-receptor antagonist, or saralasin (250 microg/kg), an angiotensin II receptor antagonist, in hemorrhaged rats partially blocked the pressor response to U-46619 (1 microg) injected into the LCV, PVN, RVLM and NTS. Results show that centrally administered U-46619, a TXA(2) analog, increases blood pressure and reverses hypotension in hemorrhagic shock. Activation of central TXA(2) receptors mediates the pressor effect of the drug. Furthermore, the increases in plasma adrenaline, noradrenaline, vasopressin levels and renin activity are involved in these effects.

Topics: 15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; Adrenergic alpha-1 Receptor Antagonists; Angiotensin II Type 1 Receptor Blockers; Animals; Antidiuretic Hormone Receptor Antagonists; Blood Pressure; Brain; Bridged Bicyclo Compounds, Heterocyclic; Catecholamines; Fatty Acids, Unsaturated; Heart Rate; Hemodynamics; Hemorrhage; Hydrazines; Hypotension; Injections; Injections, Intraventricular; Male; Medulla Oblongata; Paraventricular Hypothalamic Nucleus; Rats; Rats, Sprague-Dawley; Renin; Shock, Hemorrhagic; Solitary Nucleus; Thromboxane A2; Vasoconstrictor Agents; Vasopressins

This study investigates angiotensin II and endothelin-1 mediated mechanisms involved in the haemodynamic, hormonal, and renal response towards acute hypotensive haemorrhage.. Conscious dogs were pre-treated with angiotensin II type 1 (AT1) and/or endothelin-A (ETA) receptor blockers or not. Protocol 1: After a 60-min baseline period, 25% of the dog's blood was rapidly withdrawn. The blood was retransfused 60 min later and data recorded for another hour. Protocol 2: Likewise, but preceded by AT1 blockade with i.v. Losartan. Protocol 3: Likewise, but preceded by ETA blockade with i.v. ABT-627. Protocol 4: Likewise, but with combined AT1 plus ETA blockade.. In controls, haemorrhage decreased mean arterial pressure (MAP) by approximately 25%, cardiac output by approximately 40%, and urine volume by approximately 60%, increased angiotensin II (3.1-fold), endothelin-1 (1.13-fold), vasopressin (116-fold), and adrenaline concentrations (3.2-fold). Glomerular filtration rate and noradrenaline concentrations remained unchanged. During AT1 blockade, the MAP decrease was exaggerated (-40%) and glomerular filtration rate fell. During ETA blockade, noradrenaline increased after haemorrhage instead of adrenaline, and the MAP recovery after retransfusion was blunted. The decrease in cardiac output was similar in all protocols.. Angiotensin II is more important than endothelin-1 for the short-term regulation of MAP and glomerular filtration rate after haemorrhage, whereas endothelin-1 seems necessary for complete MAP recovery after retransfusion. After haemorrhage, endothelin-1 seems to facilitate adrenaline release and to blunt noradrenaline release. Haemorrhage-induced compensatory mechanisms maintain blood flow more effectively than blood pressure, as the decrease in cardiac output--but not MAP--was similar in all protocols.

Topics: Angiotensin II; Animals; Antihypertensive Agents; Atrasentan; Blood Pressure; Blood Transfusion; Cardiac Output; Dogs; Endothelin-1; Epinephrine; Female; Glomerular Filtration Rate; Hemodynamics; Hemorrhage; Losartan; Norepinephrine; Pyrrolidines; Receptor, Endothelin A; Stroke Volume; Urine; Vascular Resistance; Vasopressins

The aim of the present study was to compare the influence of the renin-angiotensin and sympathetic system in the process of post-haemorrhagic vasopressin release. A dialysis of the venous blood from the sella turcica region was performed in male rats under anaesthesia. The animals were divided into eight experimental groups: 1). control; 2). bleeding; 3). 20 days after superior cervical ganglionectomy; 4). 20 days after superior cervical ganglionectomy and bleeding; 5). injection of captopril; 6). injection of captopril and bleeding; 7). 20 days after superior cervical ganglionectomy and injection of captopril; 8). 20 days after superior cervical ganglionectomy, injection of captopril and bleeding. The content of vasopressin in dialysates was determined by radioimmunoassay. In control rats the release of vasopressin into dialysates was constant during 180 min of the experiment. Bleeding, as well as, superior cervical ganglionectomy caused an increase in vasopressin release. Captopril did not change vasopressin release in comparison to control group. Furthermore, vasopressin release after both, bleeding and sympathetic denervation performed simultaneously was significantly abolished. We conclude that renin-angiotensin, as well as, sympathetic nervous system are involved in the increased post-haemorrhagic vasopressin release.

Topics: Angiotensin II; Animals; Arginine Vasopressin; Captopril; Dialysis; Dialysis Solutions; Hemorrhage; Injections, Intravenous; Male; Rats; Rats, Wistar; Renin-Angiotensin System; Sella Turcica; Superior Cervical Ganglion; Sympathetic Nervous System; Time Factors; Vasopressins

Severe hypotensive haemorrhage results in a biphasic response, characterized by an initial increase in heart rate and sympathetic vasomotor activity (phase I) followed by a life-threatening hypotension, accompanied by profound sympathoinhibition and bradycardia (phase II). The phase II response is believed to be dependent on inputs from cardiopulmonary receptors, and may be triggered by the reduction in venous return and cardiac filling associated with severe haemorrhage. In this study, we tested the hypothesis that the phase II response could be reversed by venoconstriction, which is known to enhance venous return and cardiac filling, by comparing the effects of phenylephrine (which constricts veins as well as arterioles) with that of vasopressin (which constricts arterioles but not veins). In sodium pentobarbitone-anaesthetised rats, haemorrhage evoked an initial increase in heart rate (HR) and renal sympathetic activity (RSNA) followed by a large decrease in both variables to levels below the pre-haemorrhage baseline levels (phase II response). During the phase II response, an intravenous injection of phenylephrine, sufficient to restore mean arterial pressure to the pre-haemorrhage level, resulted in a gradually developing increase (over 3-4 min) in HR and RSNA back to the baseline levels. In contrast, intravenous injection of an equipressor dose of vasopressin did not result in any increase in RSNA and only a transient increase in HR. Injection of phenylephrine, but not vasopressin, also increased the pulsatile component of central venous pressure, indicative of reduced venous capacitance. The findings indicate that venoconstriction reverses the phase II sympathoinhibition and bradycardia.

Topics: Animals; Blood Pressure; Bradycardia; Heart Rate; Hemorrhage; Hypotension; Male; Phenylephrine; Rats; Rats, Sprague-Dawley; Sympathetic Nervous System; Vasoconstriction; Vasoconstrictor Agents; Vasopressins

The effect of centrally administered galanin (Gal; 100 pM i.c.v.) on the hypothalamo-neurohypophysial storage as well as blood plasma level of vasopressin and oxytocin was estimated in haemorrhaged (1 ml per 100 g b.w.) male Wistar rats. Gal i.c.v. treatment did not alter vasopressin and oxytocin content both in the hypothalamus and neurohypophysis as well as their concentration in blood plasma of not haemorrhaged rats. Haemorrhage decreased the hypothalamic and neurohypophysial vasopressin and oxytocin storage but increased the neurohormones plasma level in animals injected with vehicle solution. During the haemorrhage, the increase in plasma vasopressin and oxytocin was inhibited in rats previously treated i.c.v. with galanin. The hypothalamic and neurohypophysial vasopressin as well as oxytocin content significantly increased in animals treated with galanin and subsequently haemorrhaged. These results suggest that galanin may have a regulatory role in the hypothalamo-neurohypophysial function especially under condition of hypovolemia.

Topics: Animals; Galanin; Hemorrhage; Hypothalamo-Hypophyseal System; Male; Oxytocin; Pituitary Gland, Posterior; Rats; Rats, Wistar; Vasopressins

This study compares the haemodynamic and hormonal responses during haemorrhage of conscious dogs pre-treated with an endothelin-A (ET-A) receptor inhibitor. The dogs were studied in two different randomized groups: the control group and a group that was given the ET-A receptor antagonist ABT-627 (as a bolus of 1 mg x kg of body weight(-1) followed by 0.01 mg x kg body weight(-1) x min(-1) intravenously). The time-course was the same for both groups: after a 1 h baseline period (pre-haemorrhage), blood (25 ml x kg of body weight(-1)) was withdrawn within 5 min. Haemodynamics were continuously recorded and hormone levels measured after 1 h (post-haemorrhage). Thereafter, the blood withdrawn was retransfused within 5 min and haemodynamics again observed for 1 h (post-retransfusion). In ABT-627-treated dogs, the decrease in mean arterial pressure from 87+/-3 to 64+/-3 mmHg (P<0.05 versus pre-haemorrhage), and cardiac output from 2.1+/-0.1 to 1.3+/-0.1 l x min(-1) (P<0.05 versus pre-haemorrhage) and the increase in systemic vascular resistance from 3286+/-174 to 4211+/-230 dyn.s.cm(-5) (P<0.05 versus pre-haemorrhage) during acute haemorrhage are comparable with controls. During haemorrhage in controls, vasopressin levels increased from 0+/-0 to 13+/-2 pg x ml(-1) (P<0.05 versus pre-haemorrhage), angiotensin II levels increased from 9+/-1 to 28+/-9 pg x ml(-1) (P<0.05 versus pre-haemorrhage) and adrenaline levels increased from 134+/-22 to 426+/-74 pg x ml(-1) (P<0.05 versus pre-haemorrhage) whereas noradrenaline levels did not change (approx. 200 pg x ml(-1)). In ABT-627-treated dogs, vasopressin levels increased from 0.2+/-0.0 to 22.2+/-6.1 pg x ml(-1) (P<0.05 versus pre-haemorrhage and P<0.05 versus control), angiotensin II levels increased from 8+/-1 to 37+/-8 pg x ml(-1) (P<0.05 versus pre-haemorrhage), noradrenaline levels increased from 147+/-16 to 405+/-116 pg x ml(-1) (P<0.05 versus pre-haemorrhage) and adrenaline levels did not change (200 pg x ml(-1)) during haemorrhage. We conclude from our results that dogs receiving the selective ET-A inhibitor ABT-627 seem to show a different hormonal response after haemorrhage compared with controls, displaying considerably higher noradrenaline concentrations. Independent of ET-A receptor inhibition, cardiac output during haemorrhage was maintained within the control range. This may indicate that the organism is defending blood flow (cardiac output) over blood pressure during haemorrhage, and that this defence s

Topics: Action Potentials; Acute Disease; Angiotensin II; Animals; Atrasentan; Blood Pressure; Cardiac Output; Dogs; Endothelin Receptor Antagonists; Endothelin-1; Hemorrhage; Norepinephrine; Pyrrolidines; Random Allocation; Receptor, Endothelin A; Vascular Resistance; Vasodilator Agents; Vasopressins

Intracerebroventricular (i.c.v.) injection of choline (50-150 microg), a precursor of the neurotransmitter acetylcholine, produced a time-and dose-dependent increase in plasma vasopressin levels in conscious, freely moving rats. The increase in plasma vasopressin in response to i.c.v. choline (150 microg) was inhibited by pretreatment with the nicotinic receptor antagonist, mecamylamine (50 microg; i.c.v.), but not by the muscarinic receptor antagonist, atropine (10 microg; i.c.v). The choline-induced rise in plasma vasopressin levels was greatly attenuated by hemicholinium-3 (HC-3; 20 microg; i.c.v.), a neuronal choline uptake inhibitor. Choline (50 or 150 microg; i.c.v.) produced a much greater increase in plasma vasopressin levels in osmotically stimulated or hemorrhaged rats than in normal rats. Choline (150 microg; i.c.v.) also enhanced plasma vasopressin response to graded hemorrhage; the enhancing effect of choline was also attenuated by HC-3 (20 microg; i.c.v.). Choline and acetylcholine concentrations in hypothalamic dialysates increased significantly following i.c.v. injection of choline (150 microg). It is concluded that choline increases plasma vasopressin levels by stimulating central nicotinic receptors indirectly, through the enhancement of acetylcholine synthesis and release, and augments the ability of osmotic stimulations or hemorrhage to stimulate vasopressin release.

Topics: Acetylcholine; Animals; Choline; Dose-Response Relationship, Drug; Hemicholinium 3; Hemorrhage; Hypothalamus; Injections, Intraventricular; Male; Muscarinic Antagonists; Neurotransmitter Uptake Inhibitors; Nicotinic Antagonists; Presynaptic Terminals; Rats; Rats, Wistar; Receptors, Nicotinic; Saline Solution, Hypertonic; Synaptic Transmission; Vasopressins; Water-Electrolyte Balance

Lower body negative pressure (LBNP) reduces central venous pressure (CVP) and cardiac output. The elderly are reported to have a limited capacity to increase cardiac output by increasing heart rate (HR), are especially dependent on end diastolic volume to maintain stroke volume and therefore should be especially vulnerable to LBNP. The present study compared the effects of LBNP in the young and old. Stroke volume was assessed non-invasively as stroke distance (SD) by aortovelography. Two groups of healthy male volunteers were studied: eight young (29.7 +/- 2.0 years, mean +/- S.E.M.) and nine old (70.1 +/- 0.9 years). LBNP was applied progressively at 17.5, 35 and 50 mmHg in 20 min steps, with measurements taken during each steady state. There were similar, significant, falls in CVP in both groups. SD fell significantly in both groups from respective control values of 24.8 +/- 1.6 and 16.6 +/- 0.9 cm to 12.5 +/- 1.3 and 8.9 +/- 0.4 cm at a LBNP of 50 mmHg. Although SD in the elderly was significantly lower than in the young, the LBNP-induced changes were not different between groups. Both groups produced similar significant increases in vascular resistance, HR, plasma vasopressin (AVP) and noradrenaline. Mean arterial blood pressure (MBP) and plasma adrenaline did not change significantly. Therefore healthy old men respond to LBNP in a similar manner to the young, although MBP and SD are regulated around different baselines in the two groups.

Topics: Adult; Aged; Aging; Blood Pressure; Epinephrine; Heart Rate; Hemorrhage; Humans; Hypovolemia; Lower Body Negative Pressure; Male; Norepinephrine; Stroke Volume; Vascular Resistance; Vasopressins

We have proposed that the reflex increase in arginine vasopressin (AVP) secretion in response to hypovolemia is due to arterial baroreceptor unloading. If arterial pressure is the key to the mechanism, the slope relating plasma AVP to arterial pressure should be the same in response to hemorrhage, a model of true hypovolemia, and in response to thoracic inferior vena caval constriction (IVCC), a model of central hypovolemia. We tested this hypothesis in conscious, chronically instrumented dogs (n = 8). The mean coefficient of determination (r(2)) values obtained from the individual regressions of log AVP onto systolic pressure (SP) and mean arterial pressure (MAP) in response to hemorrhage were 0.953 +/- 0.009 and 0.845 +/- 0.047, respectively. Paired comparisons indicated a significant difference between the means (P < 0.05), hence, SP was used in subsequent analyses. The mean slopes relating the log of plasma AVP to SP in response to hemorrhage and IVCC were -0.034 +/- 0.003 and -0.032 +/- 0.002, respectively, and the means were not significantly different (P = 0.7). The slopes were not altered when the experiments were repeated during acute blockade of cardiac receptors by intrapericardial procaine. Finally, sinoaortic denervation (n = 4) markedly reduced the slope in both the hemorrhage and IVCC treatments. We conclude that baroreceptors monitoring arterial pressure provide the principal reflex control of AVP secretion in response to hypovolemia.

Topics: Anesthetics, Local; Animals; Aorta, Thoracic; Arginine Vasopressin; Atrial Function; Baroreflex; Blood Pressure; Blood Volume; Disease Models, Animal; Dogs; Female; Ganglionic Blockers; Heart Atria; Hemorrhage; Hypovolemia; Ligation; Male; Predictive Value of Tests; Procaine; Regression Analysis; Vasopressins; Vena Cava, Inferior; Ventricular Function

NG-nitro-L-arginine methyl ester (L-NAME; 250 micrograms/5 microliters), an inhibitor of NO synthase, or the vehicle artificial cerebrospinal fluid (aCSF; 5 microliters) was administered intracerebroventricularly to conscious rats hemorrhaged (0.7 ml/min) to a 20% volume depletion. Hypotension was maximal 5 min after hemorrhage ended, with compensatory recovery to basal levels 20 min later, regardless of drug treatment. L-NAME, however, elevated (P < 0.05) blood pressure (vs. aCSF controls) 40-45 min after intracerebroventricular administration. In normovolemic rats, L-NAME produced a significant pressor response and increased plasma levels of vasopressin (VP) and oxytocin (OT). After hemorrhage, both hormone levels increased, but only OT was further enhanced by L-NAME. Thus centrally produced NO tonically inhibits OT and VP secretion under basal normovolemic conditions and selectively inhibits OT release during hypovolemia. Hemorrhage increased the rates of glucose utilization in the neural lobe, indicative of enhanced efferent neural functional activity. L-NAME further enhanced the metabolic activity in the entire hypothalamoneurohypophysial system of hemorrhaged animals. Several other brain structures involved in the regulation of blood pressure and the stress response were also metabolically affected by the hemorrhage and L-NAME.

Topics: Animals; Blood Pressure; Body Fluids; Brain; Deoxyglucose; Enzyme Inhibitors; Glucose; Hemorrhage; Homeostasis; Male; NG-Nitroarginine Methyl Ester; Nitric Oxide; Oxytocin; Pituitary Gland, Posterior; Rats; Rats, Sprague-Dawley; Vasopressins

This study tests the hypothesis that conscious rabbits late in pregnancy (P), but not at midgestation (MP), are less able to maintain arterial pressure during hemorrhage. Blood volume (BV) was elevated (P < 0.05) by an average of 13 +/- 4 (MP) and 35 +/- 3% (P). Rabbits were bled in both the nonpregnant (NP) and P state at 2% of the initial BV per minute. The hemorrhage was stopped after arterial pressure decreased. In NP rabbits, arterial pressure was well maintained near control pressures of 70 +/- 2 mmHg until 38 +/- 2% of the initial BV was removed and then rapidly fell to reach a nadir at 35 +/- 2 mmHg. In contrast, in P rabbits, basal arterial pressure was lower (61 +/- 2 mmHg; P < 0.05) and gradually decreased to below control after <25% of the initial BV was removed. Moreover, the rapid hypotensive phase was triggered with a lower percent BV removal (33 +/- 2%; P < 0.05). Basal heart rate was higher during P (149 +/- 5 vs. 189 +/- 9 beats/min; P < 0.05), and reflex increases were delayed. The slope of the relationship between arterial pressure and vasopressin was not modified during P, although the line was shifted to a lower pressure (P < 0.05). Larger increases in plasma renin activity and ANG II concentration were produced during hemorrhage in P rabbits. In contrast, no differences in the changes in arterial pressure, heart rate, and vasopressin were found between NP and MP rabbits during hemorrhage, although increases in renin and ANG II were greater at MP (P < 0.05). In summary, although P conscious rabbits are less able to maintain blood pressure during hemorrhage, this change is not evident at MP. These data suggest that the factors that mediate the P-induced alterations in arterial pressure regulation are not operative until late in gestation.

Topics: Angiotensin II; Animals; Baroreflex; Blood Pressure; Blood Volume; Female; Heart Rate; Hematocrit; Hemodynamics; Hemorrhage; Pregnancy; Pregnancy Complications; Rabbits; Renin; Renin-Angiotensin System; Time Factors; Vasopressins

There is increasing evidence that ovarian steroids inhibit vascular responsiveness to the neurohypophysial hormone vasopressin. The present study examined the recovery of the arterial blood pressure following a single (2 ml/100 g body weight) haemorrhage in ovariectomized (OVX) Brattleboro rats with hereditary hypothalamic diabetes insipidus (BDI) and rats of the parent Long Evans (LE) strain. Some groups of OVX rats received subcutaneous implants of either 17 beta-oestradiol (E2) or progesterone 7 days prior to haemorrhage. The arterial blood pressure recovery immediately following haemorrhage was significantly impaired in both groups of steroid-treated OVX LE rats compared with the OVX controls (both comparisons P < 0.05). The impairment in blood pressure recovery seen in the steroid-replaced OVX LE rats was similar to that seen in pro-oestrous rats (when ovarian steroid levels are raised) compared with male rats of this strain (P < 0.05). In contrast, ovariectomy with or without steroid replacement in BDI rats had no further effect on the already attenuated recovery of arterial blood pressure after haemorrhage in this strain. Heart rate responses to haemorrhage also showed strain differences, which were dependent on steroid treatment. Pro-oestrous female LE rats showed a small decrease in heart rate after haemorrhage, followed by a recovery process, and this initial bradycardia was markedly enhanced in the OVX steroid-treated animals. In contrast, untreated OVX LE rats showed an initial and sustained increase in heart rate which was significantly higher than in the steroid-treated OVX animals (P < 0.05). All BDI rats, irrespective of treatment, consistently showed an increased heart rate after haemorrhage. In conclusion, ovarian steroid replacement in OVX LE, but not vasopressin-deficient BDI, rats was associated with an attenuated pressor recovery after haemorrhage. This provides further evidence for the existence of an important inhibitory interaction between ovarian steroids and vasopressin. The initial decrease in heart rate observed in pro-oestrous and steroid-treated OVX LE rats after haemorrhage also appears to be related to an ovarian steroid-vasopressin interaction.

Topics: Animals; Blood Pressure; Diabetes Insipidus; Estradiol; Female; Heart Rate; Hemorrhage; Male; Ovariectomy; Progesterone; Rats; Rats, Brattleboro; Rats, Inbred Strains; Rats, Mutant Strains; Vasopressins

Systemic hypotension may result in postoperative renal failure in jaundiced patients. Attenuated responsiveness to catecholamines and hypovolaemia has been reported in jaundiced animals and may be a mechanism contributing to the increased susceptibility of jaundiced patients to haemorrhagic shock. This suggests that an alternative to vasoactive amines to control perioperative hypotension could be desirable.. This study evaluated the pressor response to vasopressin in normovolaemic 3-day bile duct-ligated rats and in 3-day bile duct-ligated rats after an acute controlled haemorrhage. It also evaluated the response after volume loading with 0.9 per cent saline, 7.5 per cent saline, colloid and mannitol before controlled haemorrhage. In addition, blood volume was measured using radiolabelled albumin. All the data obtained from bile duct-ligated rats were compared with data from sham-operated animals.. Attenuated pressor responses to vasopressin were not observed in either normotensive bile duct-ligated rats or in the bile duct-ligated rats subjected to controlled haemorrhage. Volume loading with the four fluids over the dosing range 2.5-7.5 microliters per g body-weight in bile duct-ligated rats reversed the susceptibility to haemorrhagic hypotension.. Although no reduction in blood volume was demonstrated, bile duct-ligated rats may have a reduced effective blood volume manifesting itself as a latent hypovolaemia and/or tendency to hypotension. Preoperative fluid loading could be beneficial because it corrects hypovolaemia and improves cardiovascular function, as well as improving the cardiovascular response to haemorrhage.

Topics: Animals; Bile Ducts; Blood Pressure; Blood Volume; Female; Hemorrhage; Hypotension; Ligation; Random Allocation; Rats; Rats, Sprague-Dawley; Therapeutic Irrigation; Vasopressins

Elimination of baroreceptor afferent input to the brain produced by chronic lesion of nucleus of the solitary tract (NTS) does not alter vasopressin (VP) release during hypotensive hemorrhage in conscious rats. To investigate whether the kidneys play a critical role in stimulating VP release during hemorrhage in chronic NTS-lesioned rats, we examined the effects of removing potential signals arising from the kidneys. In NTS-lesioned rats, nephrectomy or renal denervation, but not captopril injection, markedly attenuated (but did not abolish) hemorrhage-induced VP release. In contrast, none of these manipulations attenuated the VP response in NTS-intact rats. Hemorrhage increased plasma renin activity in control and NTS-lesioned rats, and this response was not altered by renal denervation. In rats with NTS lesions and renal denervation, hemorrhage induced the expression of Fos in hypothalamic magnocellular VP neurons in a pattern similar to that of hemorrhage in intact rats. Collectively, these results indicate that in chronic NTS-lesioned rats an afferent signal arising from the kidneys stimulates VP release during hemorrhage, possibly through renal nerves. However, with the NTS intact or after the selective removal of arterial baroreceptor inputs, such a role for the kidneys is not apparent. Furthermore, in the absence of the NTS and renal nerves, another signal generated by hypotensive hemorrhage continues to stimulate VP neurons.

Topics: Animals; Captopril; Hemorrhage; Kidney; Male; Nephrectomy; Paraventricular Hypothalamic Nucleus; Proto-Oncogene Proteins c-fos; Rats; Rats, Sprague-Dawley; Solitary Nucleus; Supraoptic Nucleus; Vasopressins

Vasovagal reflexes, such as hypotension and bradycardia, are induced by rapid hemorrhage and mimic neurocardiogenic reflexes in mammals. We examined the role of vasopressin in the neurocardiogenic responses to mild, rapid hemorrhage (1 mL/100 g for 30 seconds) and severe hemorrhage (1 mL/100 g body wt for 30 seconds repeated three times at 11-minute intervals) in homozygous Brattleboro and Long-Evans rats. Mild, rapid hemorrhage induced severe bradycardia and hypotension only in Long-Evans rats. Exogenous vasopressin (1.85 pmol/kg per minute for 1 hour) restored both the bradycardic and hypotensive responses in Brattleboro rats. DDAVP, a vasopressin V2-receptor agonist (0.19 pmol/kg per minute for 24 hours), did not affect the cardiovascular responses to hemorrhage in Brattleboro rats, although it maintained urine production within normal limits. However, OPC-31260 (21.6 mumol/kg IV), a vasopressin V2-receptor antagonist, attenuated both the hypotensive and bradycardic responses to hemorrhage in Long-Evans rats. A vasopressin V1-receptor antagonist attenuated bradycardia and delayed the recovery of arterial pressure after hemorrhage but did not affect the hypotension that occurred immediately after hemorrhage in Long-Evans rats. Methylatropine also attenuated both the bradycardic and hypotensive responses induced by hemorrhage, but propranolol had no effect on the cardiovascular responses to hemorrhage in Long-Evans rats. The recovery of arterial pressure after repeated hemorrhage was less adequate in Brattleboro rats than in Long-Evans rats. Our results suggest that the neurocardiogenic responses to hemorrhage, especially hypotension, may be related to vasodilation induced by a V2-receptor-mediated mechanism and by the vagal reflex, both of which are substantiated by the existence of vasopressin. The coexistence of V1- and V2-receptor mechanisms may be necessary for the hypotensive response to hemorrhage. We found that a V2-receptor antagonist attenuated the hypotension mediated by the so-called neurocardiogenic reflex.

Topics: Acute Disease; Animals; Antidiuretic Hormone Receptor Antagonists; Arginine Vasopressin; Autonomic Nerve Block; Benzazepines; Cardiovascular System; Deamino Arginine Vasopressin; Diabetes Insipidus; Heart; Hemorrhage; Male; Nervous System; Rats; Rats, Brattleboro; Rats, Inbred Strains; Receptors, Vasopressin; Recurrence; Vasopressins

Intracerebroventricular (i.c.v.) infusion of hypertonic NaCl improves the tolerance to haemorrhage in sheep. Since i.c.v. angiotensin II (ANG II) shares many of the effects of hypertonic NaCl on fluid balance control and blood pressure, we aimed to determine whether i.c.v. ANG II would also be effective in that regard. Six adult conscious ewes were bled from the jugular vein until the mean arterial pressure suddenly dropped to between 45 and 50 mmHg, during an i.c.v. infusion of ANG II (2 pmol kg-1 min-1) which commenced 30 min prior to start of blood removal and continued until end of retransfusion about 80 min after haemorrhage. A corresponding haemorrhage in the same animals during an i.c.v. infusion of 0.9% NaCl served as controls. Significantly more blood had to be withdrawn to induce hypotension when ANG II was given i.c.v. (22.3 +/- 1.8 vs. 12.6 +/- 1.2 mL kg-1). The degree of hypotension and the recovery rate of the blood pressure did not differ between the experiments. The increased tolerance to blood loss by ANG II i.c.v. was accompanied by a reinforced elevation of the systemic vascular resistance and a larger decline of the cardiac output. The plasma norepinephrine concentration was significantly increased immediately after haemorrhage during i.c.v. ANG II, but not in control experiments. The overall vasopressin response to the hypotensive blood loss was not affected by ANG II, but high plasma levels were obtained already during the non-hypotensive stage of haemorrhage. The i.c.v. infusion of ANG II caused a significant lowering of the plasma protein concentration before start of bleeding and accentuated the haemodilution caused by the haemorrhage. We conclude that central administration of ANG II increases the tolerance to haemorrhage in sheep but with concomitant haemodynamic changes which appear unfavourable regarding cardiac load and tissue perfusion.

Topics: Angiotensin II; Animals; Blood Pressure; Blood Proteins; Cardiac Output; Female; Hematocrit; Hemodynamics; Hemorrhage; Injections, Intraventricular; Norepinephrine; Renin; Sheep; Sodium; Vascular Resistance; Vasoconstrictor Agents; Vasopressins

It is now clear that ATP acts as a neurotransmitter in both the peripheral and central nervous systems. In the periphery, purinergic transmission has been best studied at certain sympathetic neuroeffector junctions where ATP, co-localized with noradrenaline, is used to elicit the primary post-junctional response. More recently, several groups have raised the possibility that central catecholaminergic neurons might use ATP in a similar fashion. Accordingly, we now present findings from immediate early gene expression and electrophysiological studies which indicate that ATP, acting through P2 purinoreceptors, is used as a transmitter by caudal brainstem noradrenergic neurons, the A1 group, in their interaction with vasopressinergic neurosecretory cells. Supraoptic nucleus vasopressin cell responses to moderate haemorrhage, known to be generated by the A1 projection, were suppressed by hypothalamic application of the P2 receptor antagonist suramin. However, suramin did not alter vasopressin cell responses to osmotic challenge or severely hypotensive haemorrhage, two stimuli known to excite vasopressin cells independently of the A1 projection. These data are consistent with an identity of action between the A1 input to vasopressin cells and the activation of ATP receptors on vasopressin cells. The use of ATP as a transmitter by other catecholamine neurons in the brain awaits further confirmation, but the present findings suggest that in certain instances the therapeutic manipulation of central catecholamine neuron output might best be achieved with pharmacological agents which target purinergic rather than adrenergic transmission.

Topics: Adenosine Triphosphate; Adrenergic Fibers; Animals; Blood Pressure; Hemorrhage; Hypothalamus; Proto-Oncogene Proteins c-fos; Suramin; Vasopressins

This study investigated the role of brain angiotensin (Ang II) in thirst induced by hemorrhage. Hemorrhage by blood withdrawal from the femoral artery to 33% and 44% blood volume loss produces a dose response increase in plasma Ang II. In the brainstem there was no Ang II response to hemorrhage. In the hypothalamus, Brain Ang II was maximally elevated to 33% hemorrhage. Thus, plasma Ang II and brain Ang II had an independent response to hemorrhage. To further test the role of central versus peripheral Ang II, we tested the effect of central (50 mg) and peripheral (50 mg/kg) administration of captopril or central injection of 1 mg losartan or 3 mg CGP 42112A prior to a 33% hemorrhage in unanesthetized male Sprague-Dawley rats (250 g). Drinking was measured and AVP blood samples were taken before and after hemorrhage. The results show that central (i.v.t.) administration of captopril and losartan inhibited drinking compared to controls (0.33 +/- 0.3 ml vs. 2.3 +/- 0.8 ml: P < 0.05 and 0.20 +/- 0.09 ml vs.3.05 +/- 0.81 ml; P < 0.01, respectively) while peripheral (i.p.) captopril alone increased drinking in response to hemorrhage (5.81 +/- 0.81 ml vs. 2.3 +/- 0.8 ml; P < 0.05). AVP levels were elevated at 5 and 15 min, but neither injections of losartan or CGP 42112A i.v.t. affected this response to hemorrhage. We conclude that increased hypothalamic brain Ang II after hypovolemic hemorrhage stimulates thirst and blood pressure restoration and acts through AT1 receptors. The release of AVP in hemorrhage, however, does not rely exclusively on the angiotensinergic pathway in the brain.

Topics: Angiotensin II; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Animals; Biphenyl Compounds; Blood Pressure; Blood Volume; Captopril; Cohort Studies; Colony-Stimulating Factors; Drinking; Hemorrhage; Hypothalamus; Imidazoles; Injections, Intraperitoneal; Injections, Intraventricular; Losartan; Male; Oligopeptides; Radioimmunoassay; Rats; Rats, Sprague-Dawley; Receptors, Angiotensin; Recombinant Proteins; Tetrazoles; Thirst; Time Factors; Vasopressins

The acute effects of haemorrhage (15 ml (kg body wt)-1) on renal function at whole-kidney and single-nephron levels were studied in Inactin-anaesthetized rats. In order to assess the role of vasopressin in mediating the haemodynamic effects, responses in untreated Long-Evans rats were compared with those in Brattleboro rats (which lack circulating vasopressin) and in Long-Evans rats treated with a V1 receptor antagonist. In time-control animals, there were no significant changes in mean arterial pressure (MAP), excretion rates, glomerular filtration rate (GFR), superficial-nephron GFR (SNGFR) or fluid reabsorption in the superficial proximal tubules during the course of the experiment. Following haemorrhage, the immediate reduction in MAP was followed in each group by partial recovery for 30 min; thereafter, MAP was stable. In untreated Long-Evans rats, haemorrhage was followed by a 26% reduction in GFR (P < 0.001, measured 60-150 min post-haemorrhage) and a larger reduction (45%, P < 0.001) in SNGFR, so that the SNGFR/GFR ratio fell significantly ((27.9 +/- 1.9) x 10(-6), control period; (20.2 +/- 2.2) x 10(-6) post-haemorrhage, P < 0.01). Slightly greater reductions in GFR and SNGFR were seen in Brattleboro rats and V1 antagonist-treated Long-Evans rats, which corresponded to slightly greater haemorrhage-induced reductions in blood pressure in these groups; the falls in the SNGFR/GFR ratio were similar to that in untreated Long-Evans rats. In all three groups of bled rats, fractional reabsorption by the proximal convoluted tubule increased slightly 30-60 min after haemorrhage, but during the subsequent period (60-150 min) returned to values indistinguishable from those during the control period. The results suggest that the renal haemodynamic changes that follow moderate haemorrhage include a preferential reduction in the GFR of superficial nephrons. Vasopressin appears to play no role in this response. Increases in fractional reabsorption in the proximal tubules are seen only during the immediate post-haemorrhage period.

Topics: Absorption; Animals; Blood Pressure; Diuresis; Glomerular Filtration Rate; Hemorrhage; Kidney; Kidney Tubules, Proximal; Male; Natriuresis; Nephrons; Potassium; Punctures; Rats; Rats, Brattleboro; Rats, Inbred Strains; Vasopressins

To study the relationship between blood volume and the plasma level of endothelin-1 (ET-1), we examined the effects of blood volume depletion and expansion on the plasma ET-1 level in the rat. Anesthetized Wistar rats were subjected to hemorrhage (7 ml/kg), blood transfusion (7 ml/kg), or sham treatment. The same blood volume depletion and expansion were performed in other groups of rats, after bilateral cervical vagotomy or administration of intravenous atropine, to examine the role of the cardiopulmonary baroreflex. Hemorrhage produced mild decreases in the central venous pressure and arterial blood pressure, and an increase in the heart rate. Blood transfusion caused the opposite responses. The plasma ET-1 level was significantly higher in the volume-depleted rats (4.7 +/- 0.4 pg/ml, mean +/- SE, p < 0.05 vs. control), and was lower in the volume-expanded rats (2.6 +/- 0.2 pg/ml, p < 0.05) than in the control group (3.5 +/- 0.3 pg/ml). In the vagotomized rats, the blood volume depletion decreased and the volume expansion increased the central venous pressure and the arterial pressure, but they did not change the heart rate or the plasma ET-1 level. Vagal efferent inhibition with atropine did not affect the volume-induced changes in the plasma ET-1 level. These results indicate that the plasma level of ET-1 increases with blood volume depletion, and decreases with volume expansion. The cardiopulmonary baroreflex may play an important role in the regulation of plasma ET-1 levels when the blood volume is altered.

Topics: Animals; Baroreflex; Blood Pressure; Blood Transfusion; Blood Volume; Central Venous Pressure; Endothelins; Epinephrine; Heart Rate; Hemorrhage; Male; Norepinephrine; Rats; Rats, Wistar; Renin; Vagotomy; Vasopressins

c-fos expression mapping and electrophysiological recording experiments were done to clarify the role of the A1 noradrenergic cell group in the vasopressin response to hypotensive hemorrhage. In pentobarbital-anesthetized rats, moderate and severe hypotensive hemorrhages were simulated by brief occlusion of the inferior vena cava sufficient to reduce mean arterial pressure to approximately 50 or 30 mmHg, respectively. Both stimuli significantly increased the number of A1 region catecholamine cells displaying Fos-like immunoreactivity, this effect being most prominent at the level of the area postrema. Both stimuli also increased the number of supraoptic nucleus vasopressin cells displaying Fos-like immunoreactivity. Accordingly, electrophysiological studies involving separate animals confirmed that both moderate and severe caval occlusion significantly increased the firing of functionally identified vasopressin cells recorded in the supraoptic nucleus. However, although interruption of A1 region neuronal function by injection of gamma-aminobutyric acid at the level of the area postrema eliminated the increase in vasopressin cell firing elicited by moderate caval occlusion, it did not block the response to severe caval occlusion. These findings suggest that, in the rat, the vasopressin response to an acute reduction in central blood volume, such as that produced by hemorrhage, depends on the A1 projection only if the stimulus is of moderate intensity. Severe stimuli appear to involve activation of both the A1 projection and an additional vasopressin-stimulatory pathway that bypasses the A1 region.

Topics: Animals; Catheterization; gamma-Aminobutyric Acid; Hemorrhage; Injections; Male; Medulla Oblongata; Neurons; Norepinephrine; Pituitary Gland, Posterior; Proto-Oncogene Proteins c-fos; Rats; Rats, Wistar; Vasopressins; Venae Cavae

Hemorrhage induces a rapid redistribution of protein from extravascular spaces into the blood. We studied the effects of acute, nontraumatic hemorrhage on tracer-albumin clearances into individual tissues of rats to determine if reduced protein extravasation could account for intravascular protein gain. Three groups were studied: 1) HEM animals were anesthetized with pentobarbital sodium and bled to a mean arterial pressure of 50 mmHg for 90 min; 2) HEM-RS animals were treated identical to group 1 and then resuscitated with 5% bovine serum albumin (BSA) until baseline arterial pressures were regained; 3) SHAM animals served as time controls. Hemodynamic variables were measured periodically throughout hemorrhage and clearance periods, and plasma samples were collected prior to death for protein and hormone analysis. Plasma clearance of 131I-BSA into individual tissues was measured over the final 30 min of each protocol with a terminal injection of 125I-BSA used to correct for intravascular volume. Reduction of blood volume by 35% in HEM-treated animals resulted in a marked decrease in albumin transport relative to the SHAM group (p < or = .05) in the following tissues: skeletal muscle (-65%), skin (-49%), ileum (-75%), cecum (-66%), colon (-67%), heart (-67%), and lung (-71%). Significant changes were not observed in the remaining tissues sampled: pancreas, kidney, and cerebrum. Albumin clearances in the HEM-RS group were slightly but not significantly lower than SHAM animals except for skeletal muscle, where transport remained depressed following resuscitation.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Acute Disease; Animals; Atrial Natriuretic Factor; Biological Transport; Blood Glucose; Blood Volume; Body Water; Body Weight; Brain; Colon; Coronary Vessels; Disease Models, Animal; Extravascular Lung Water; Hematocrit; Hemodynamics; Hemorrhage; Ileum; Lung; Male; Osmolar Concentration; Plasma Volume; Rats; Rats, Wistar; Resuscitation; Serum Albumin; Skin; Tissue Distribution; Vasopressins

In rats, secretion of vasopressin initiated by hemorrhage was completely abolished after muscimol-induced inhibition of neuronal function in the A1 region of the ventrolateral medulla oblongata. The A1 neurons are essential links in the central pathway to hypothalamic vasopressin-synthesizing neurons in this species.

Topics: Animals; Hemorrhage; Male; Medulla Oblongata; Microinjections; Muscimol; Rats; Rats, Inbred Strains; Vasopressins

Experiments were carried out, using the technique of in vivo microdialysis in conscious rats, to determine whether hemorrhage, a potent stimulus for the release of vasopressin from the posterior pituitary into the circulation, would also result in a local release of vasopressin from the paraventricular nucleus (PVN), and whether this release is affected by gender. Male and non-estrous female rats were prepared with a microdialysis probe adjacent to the PVN and femoral arterial and venous catheters the day before the experiment. On the day of the experiment, rats was bled either 20% or 30% of blood volume. The concentration of vasopressin in the dialysate increased significantly in the males following both hemorrhages and in the females following the 30% hemorrhage. There were no statistically significant differences in the post-hemorrhage dialysate vasopressin concentration with respect to either gender or magnitude of the hemorrhage. The plasma vasopressin concentration increased markedly in response to the hemorrhage and this response was greater in females following the 30% hemorrhage. There were no gender differences in the reduction in arterial pressure following either hemorrhage. It is concluded that physiological stimuli for the release of vasopressin into the circulation also result in intrahypothalamic release of this hormone.

Topics: Animals; Blood Pressure; Female; Heart Rate; Hemorrhage; Male; Microdialysis; Osmolar Concentration; Paraventricular Hypothalamic Nucleus; Rats; Rats, Sprague-Dawley; Sex Characteristics; Vasopressins

The present study compared Fos expression in identified hypothalamic magnocellular neurons in lactating and non-lactating female rats submitted to acute haemorrhage or 24 h of water deprivation, stimuli that induce the release of both oxytocin and vasopressin. Quantitative analysis of preparations doubly immunostained for Fos and either of the neuropeptides revealed that oxytocin and vasopressin neurons synthesise Fos in response to either stimulus but to a different degree, depending on the type of neuron, the type of stimulus, the location of the neurons and the reproductive state of the animal. Thus, in terms of number of cells, haemorrhage was significantly more potent than water deprivation in inducing Fos immunoreactivity in either type of neuron in the supraoptic, paraventricular and anterior commissural nuclei. However, the Fos reaction of vasopressin cells in response to either stimulus was greater than that of oxytocin cells in the supraoptic and paraventricular nuclei, and in the perifornical posterior nucleus and nucleus circularis in response to water deprivation. Moreover, when considering each neuronal population as a whole, it was obvious that Fos synthesis varied in relation to the location of the neurons in the different hypothalamic nuclei, suggesting the existence of functionally distinct neuronal subgroups. Finally, our analyses clearly indicated that Fos synthesis in either type of magnocellular neuron was closely linked to the reproductive state of the animal since after haemorrhage or water deprivation, the number of Fos-positive oxytocin cells in the supraoptic nucleus and Fos-positive vasopressin cells in the paraventricular nucleus was significantly less in lactating than in virgin rats.

Topics: Animals; Female; Hemorrhage; Hypothalamus; Immunohistochemistry; Lactation; Neurons; Oxytocin; Paraventricular Hypothalamic Nucleus; Phenotype; Pregnancy; Proto-Oncogene Proteins c-fos; Rats; Rats, Wistar; Reproduction; Supraoptic Nucleus; Vasopressins; Water Deprivation

The effects of endogenous or exogenous vasopressin in models of gastric mucosal injury with a different pathophysiology (ethanol, indomethacin, reserpine, cold-restraint stress and haemorrhagic shock-induced lesions) were investigated in rats. [Mca1,TyrMe2,Arg8]vasopressin, a vasopressin pressor (V1) receptor antagonist, was found to reduce dose dependently the extent of the lesions in all models, and to protect the deeper layer of the mucosa (assessed by histology). Endogenous vasopressin deficiency, as in Brattleboro homozygous rats, had a similar effect. [Lys8]Vasopressin injected exogenously aggravated all types of lesions in normal rats. Circulating vasopressin levels were increased by ethanol, reserpine, cold-restraint stress and haemorrhagic shock, but not by indomethacin, whereas the intramucosal vasopressin content was found to be elevated in all models. Additionally, specific binding sites for vasopressin were shown on the blood vessels of the gastric mucosa (assessed by autoradiography). It is concluded that vasopressin plays a significant aggressive role in the generation of these types of lesions.

Topics: Animals; Arginine Vasopressin; Autoradiography; Cold Temperature; Disease Models, Animal; Dose-Response Relationship, Drug; Ethanol; Female; Gastric Mucosa; Hemorrhage; Indomethacin; Lypressin; Rats; Rats, Wistar; Reserpine; Vasopressins

Hypotensive hemorrhage is a major stimulus for vasopressin (VP) release, but in rats it is uncertain which receptors initiate this response. We have investigated this issue using transient occlusion of the inferior vena cava to simulate hypotensive hemorrhage. Single-unit recording experiments done in the supraoptic nucleus of pentobarbital-anesthetized rats demonstrated that severe caval occlusion, sufficient to drop mean arterial pressure (MAP) below 30 mmHg, excited 88% of putative VP neurosecretory cells and a similar proportion of putative oxytocin (OT) cells. Responsive VP cells increased their firing by 8.5 +/- 0.6 spikes/s within 11.2 +/- 0.8 s of the fall in MAP. This response was unrelated to the size of the fall in MAP and was unchanged by combined sinoaortic denervation (SAD) and vagal denervation, by T1 spinal section, or by administration of the angiotensin-converting enzyme inhibitor captopril, except that spinal section decreased the response latency. Moderate caval occlusion, sufficient to drop MAP to approximately 50 mmHg, did not excite any of the OT cells tested but did excite 65% of VP cells, causing a 3.8 +/- 0.3 spikes/s increase in firing after a delay of 9.0 +/- 1.3 s. This response was proportional to the size of the preceding fall in MAP, and after combined SAD and vagal denervation only 20% of VP cells still responded. Elimination of sinoaortic or vagal afferents alone had no effect on VP cell responses to moderate caval occlusion, except that SAD significantly increased the response latency. These data suggest that in rat the mechanisms that initiate the VP response to hypotensive hemorrhage depend on stimulus intensity.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Action Potentials; Animals; Blood Pressure; Captopril; Denervation; Electric Stimulation; Hemorrhage; Hypotension; Male; Metaraminol; Rats; Rats, Wistar; Sinoatrial Node; Spinal Cord; Supraoptic Nucleus; Vagus Nerve; Vasopressins

The present study examined the hypothesis that hypovolemia stimulates vasopressin (VP) secretion by removing tonic inhibitory baroreceptor input. Serial hemorrhage (4 samples of 2 ml/300 g body wt taken every 10 min) increased plasma VP levels in conscious rats devoid of cardiac and arterial baroreceptor reflex responses due to chronic bilateral lesions of nucleus tractus solitarius (NTS). The VP response to hemorrhage was similar to that seen in control rats and chronic sinoaortic-denervated (SAD) rats. After subcutaneous injection of 30% polyethylene glycol, NTS-lesioned rats, SAD rats, and control rats had elevated VP levels that correlated with the induced depletion of plasma volume. Additionally, in alpha-chloralose-anesthetized control rats, chronic SAD rats, and chronic NTS-lesioned rats, bilateral vagotomy had minimal effects on basal VP levels, and vagotomy in chronic NTS-lesioned rats did not prevent hemorrhage-evoked increases in VP secretion. These results do not support the idea that hemorrhage-induced VP secretion occurs through reduction in tonic inhibitory baroreceptor input. Instead, neither cardiac nor arterial baroreceptor input appears to be necessary for hypovolemia-induced VP secretion in rats.

Topics: Animals; Baroreflex; Blood Pressure; Blood Volume; Denervation; Heart Rate; Hemorrhage; Male; Polyethylene Glycols; Rats; Rats, Sprague-Dawley; Sinoatrial Node; Solitary Nucleus; Stereotaxic Techniques; Time Factors; Vasopressins

Our previous data showed that the pancreatitis induced in rats by cerulein develops into hemorrhagic pancreatitis following water-immersion stress. The present study examined the effects of water-immersion stress and high doses of cerulein (intraperitoneal injection) on pancreatic blood flow. Five hours of water-immersion stress reduced the local pancreatic blood flow to approximately 30% of the initial value (253.75 +/- 12.58 ml/min/100 g) without causing any histological alterations. Blood flow was decreased as early as 1 h after the immersion and reached the lowest value (30% of initial value) 3 h after the immersion. The administration of 40 micrograms/kg body wt cerulein as two intraperitoneal injections reduced the pancreatic blood flow by 40% 5 h after the first cerulein injection. The injections of cerulein combined with water-immersion stress did not reduce the pancreatic blood flow more than did water-immersion stress alone. The systemic blood pressure was unaffected during 5 h of water immersion after the cerulein injections. These findings suggest that in rats the stress-induced decrease of local pancreatic blood flow may not produce pancreatitis, but may aggravate an existing acute pancreatitis.

Topics: Amylases; Animals; Capillaries; Dopamine; Endothelium, Vascular; Hemorrhage; Male; Organ Size; Pancreas; Pancreatitis; Rats; Rats, Sprague-Dawley; Regional Blood Flow; Stress, Physiological; Thrombosis; Vasopressins

The effects of iso- and hypo-osmotic reduction of the CSF [Na+] on the tolerance to blood loss and concomitant cardiovascular and humoral responses were studied in conscious sheep. Animals only subjected to haemorrhage served as controls. The changes in CSF composition were induced by intracerebroventricular infusions of 0.3 M mannitol, respectively, 0.04 M NaCl. In the former instance the CSF [Na+] was reduced by 18 mM whereas a lowering by 13 mM concomitant with decreased CSF osmolality (mean change 25 mOsm kg-1) was seen in response to the NaCl solution. Apart from a slight lowering of the cardiac output during the infusion of 0.3 M mannitol preceding haemorrhage, the changes in CSF composition did not have any significant haemodynamic effects in the normovolaemic animal, or altered the cardiovascular responses to a subsequent hypotensive haemorrhage. The amount of blood needed to be withdrawn to obtain the predefined degree of hypotension did not differ significantly between treatment groups. The plasma vasopressin and angiotensin II concentrations were consistently increased by the hypotensive haemorrhage, but the magnitude of the vasopressin response was significantly reduced when the CSF [Na+] was lowered. We conclude that lowered CSF [Na+] and/or osmolality, in contrast to increased CSF [Na+], does not influence the tolerance to blood loss or the accompanying haemodynamic changes in sheep, in spite of an attenuated vasopressin response.

Topics: Angiotensin II; Animals; Consciousness; Female; Hemodynamics; Hemorrhage; Hypotension; Injections, Intraventricular; Mannitol; Osmolar Concentration; Potassium; Renin; Sheep; Sodium; Sodium Chloride; Vasopressins

The experiments were designed to determine whether potassium-loaded rats have a deficient recovery of blood pressure after a rapid arterial haemorrhage. Potassium loading was achieved by providing a 0.75% KCl solution as drinking fluid for 14 days, while control rats had either distilled water or tapwater. MAP, HR, Hct, and plasma electrolytes were determined before and after 1 and 2% body weight haemorrhage in anaesthetized Sprague-Dawley rats. Potassium-loaded rats had significantly reduced blood pressure recovery within 20 min after haemorrhage. HR was significantly reduced within 5 min only after 2% haemorrhage in potassium-adapted rats. Haemorrhage induced significant hyperkalaemia which was greater and significantly prolonged after 2% haemorrhage. The significant fall in Hct after haemorrhage was not affected by the magnitude of haemorrhage. In an additional group of rats, the pressor response to intravenous infusion of vasopressin was unaffected by potassium loading, whereas that to noradrenaline and angiotensin II was significantly reduced throughout the 20 min of infusion. The peak increase in blood pressure after phenylephrine injection was, however, unaffected by potassium loading. Basal plasma catecholamines concentration as well as concentrations after 1% haemorrhage were unaffected by potassium loading. It is concluded that the reduced vascular response to noradrenaline and angiotensin contributed to the reduced recovery of blood pressure after haemorrhage in potassium-loaded rats. Furthermore, the result with phenylephrine suggest a mechanism that is unrelated to direct vascular effects of noradrenaline and angiotensin II.

Topics: Acute Disease; Adaptation, Physiological; Anesthesia; Angiotensin II; Animals; Blood Pressure; Cardiovascular Physiological Phenomena; Catecholamines; Hemodynamics; Hemorrhage; Infusions, Intravenous; Male; Norepinephrine; Potassium; Rats; Rats, Sprague-Dawley; Vasopressins

The effect of haemorrhage and melatonin on the vasopressin and oxytocin storage in the neurohypophysis of pinealectomized male rats was determined. Sham operated or pinealectomized rats as well as rats pinealectomized and injected with melatonin (100 micrograms/100 g b. w., once daily over 8 days) or with melatonin vehicle (2.2% ethanol in 0.9% NaCl) were subsequently subjected to haemorrhage. Pinealectomy was followed by known decrease of both vasopressin and oxytocin content in the neurohypophysis as compared to sham operated rats. Similarly, haemorrhage decreased the neurohypophysial vasopressin and oxytocin storage in both sham operated and pinealectomized animals. Melatonin, injected to pinealectomized animals, did not modify the diminution of neurohypophysial vasopressin and oxytocin content caused by bleeding. The results demonstrate that in pinealectomized rats melatonin does not affect the rate of the response of vasopressinergic and oxytocinergic neurones to bleeding.

Topics: Animals; Hemorrhage; Male; Melatonin; Oxytocin; Pineal Gland; Pituitary Gland, Posterior; Rats; Rats, Wistar; Vasopressins

The effect of haemorrhage (1 ml per 100 g b. w.) on the vasopressin and oxytocin storage in the hypothalamus and neurohypophysis of melatonin-treated male rats was determined. Melatonin treatment (100 micrograms/100 g b. w., once daily over 8 days) resulted in a known decrease of vasopressin as well as oxytocin content both in the hypothalamus and neurohypophysis. Haemorrhage decreased the neurohypophysial vasopressin and oxytocin storage in animals injected with vehicle solution or otherwise not treated. In melatonin-treated rats, however, bleeding did not affect the actual (i.e., decreased by melatonin) vasopressin and oxytocin content in the hypothalamo-neurohypophysial system. The results demonstrate that melatonin may be involved in mechanisms determining the rate of the response of vasopressinergic and oxytocinergic neurones to bleeding.

Topics: Animals; Hemorrhage; Hypothalamus; Male; Melatonin; Oxytocin; Pituitary Gland, Posterior; Rats; Rats, Wistar; Vasopressins

During initial stages of hemorrhage in the rat, cardiovascular compensation leads to a tachycardia (mean +/- SE, 5.2 +/- 0.7%; n = 23) that helps prevent a large fall in blood pressure. This compensatory phase is followed by a decompensatory phase in which mean arterial pressure and heart rate fall. A rise in arginine vasopressin (AVP) levels has been postulated as the cause of this hemorrhage-induced bradycardia (HIB). The object of the present study was to determine whether interference with AVP release by alcohol anesthesia or neurohypophysectomy or by blockade of AVP receptors in the plasma or cerebral spinal fluid could attenuate HIB. Male Wistar rats were anesthetized with pentobarbital, surgically prepared, and bled to maintain a blood pressure of 40-50 mm Hg. After hemorrhage, heart rate decreased 15 +/- 2% (n = 6) with alcohol anesthesia compared with 32 +/- 3% (n = 7) with pentobarbital. After neurohypophysectomy, however, HIB remained unchanged (-15 +/- 2%; n = 5) compared with sham-operated controls (-19 +/- 3%; n = 6). Peripheral administration of two nonselective V1/V2 antagonists and one V2 antagonist had no effect on HIB, whereas a V1 antagonist significantly attenuated the heart rate decrease (-15 +/- 4%; n = 6) compared with controls (-32 +/- 3%; n = 7). None of the AVP antagonists tested at one tenth the peripheral dose had any effect on HIB when administered into the lateral ventricle of the brain, although a mixed serotonin, dopamine, and catecholamine antagonist, spiperone, potentiated the response. It was concluded that although peripheral release of AVP may be partially involved in the heart rate response to hemorrhage, central AVP release and central AVP receptors were not involved in HIB.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Drinking; Electrocardiography; Ethanol; Heart Rate; Hemorrhage; Male; Pentobarbital; Pituitary Gland, Posterior; Rats; Rats, Wistar; Receptors, Angiotensin; Receptors, Vasopressin; Spiperone; Vasopressins

We examined the effect of acute hypotensive hemorrhage on corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) messenger RNAs (mRNAs) in neurons of the rat hypothalamus. Sprague-Dawley male rats were cannulated (femoral artery and vein) and received a 15 ml/kg.3 min hemorrhage on the morning of the fourth day. Time controls received no hemorrhage. After light halothane anesthesia, the rats were decapitated at 1 or 4 h (six to nine rats per group). The hypothalami were removed, frozen, and sectioned at 12 microns. In situ hybridization was performed using two 48-base oligodeoxynucleotide probes for CRH and AVP message, respectively. Hemorrhage led to a fall in arterial blood pressure and heart rate that recovered by 1 h. Plasma ACTH, corticosterone, and AVP were elevated 20, 60, and 90 min after hemorrhage, but returned to near control levels by 4 h. CRH mRNA was significantly elevated 1 and 4 h after hemorrhage, as compared to time controls, in parvocellular neurons of the paraventricular nuclei. However, AVP mRNA was not different from controls at 1 or 4 h after hemorrhage in the magnocellular or parvocellular paraventricular nuclei, or in the supraoptic or accessory nuclei of the hypothalamus. AVP mRNA was also found in neurons of the suprachiasmatic nuclei, but there was no difference in the amount of mRNA between the 1-h hemorrhage and control groups. These data suggest that neural signals, originating for cardiovascular receptors activated by hemorrhage, up-regulate message for CRH but not for AVP in the paraventricular nuclei of the rat hypothalamus.

Topics: Adrenocorticotropic Hormone; Animals; Arginine Vasopressin; Corticosterone; Corticotropin-Releasing Hormone; Hemorrhage; Hypotension; Hypothalamus; Male; Rats; Rats, Inbred Strains; Receptors, Cell Surface; RNA, Messenger; Vasopressins

We determined, in urethan-anesthetized rabbits, whether pharmacological alteration of neuronal function in the ventrolateral medulla oblongata, including the A1 area, and in the nucleus tractus solitarii (NTS), alters plasma adrenocorticotropic hormone (ACTH) and vasopressin and whether inhibition of neuronal function in the ventrolateral medulla impairs the secretion of ACTH normally observed in response to hemorrhage or constriction of the inferior vena cava. We also tested whether the increase in plasma ACTH and vasopressin after pharmacological inhibition of neuronal function in the NTS is dependent on a pathway that synapses in the A1 area of the ventrolateral medulla. Activation of the A1 area with bicuculline increased both ACTH and vasopressin. Inhibition of the NTS with muscimol increased levels of both hormones, as did hemorrhage and constriction of the inferior vena cava. Inhibition of neuronal function within the A1 area with muscimol eliminated the secretion of vasopressin but did not significantly alter the secretion of ACTH, obtained by injecting muscimol into the NTS. Injection of muscimol into the A1 area eliminated the secretion of both ACTH and vasopressin in response to constriction of the inferior vena cava and, in the case of vasopressin, in response to hemorrhage. Although hemorrhage-initiated secretion of ACTH was significantly reduced by injection of muscimol into the A1 area, it was not completely eliminated by these injections or by injections of muscimol into a more rostrocaudally extensive region of the medulla oblongata. We conclude that the net output from the NTS tonically inhibits secretion of both ACTH and vasopressin, reflecting tonic baroreceptor tone. For vasopressin, the pathway from the NTS to the hypothalamus is dependent on a synapse in the A1 area. For ACTH, there are pathways to the hypothalamus that do not synapse in the A1 area, but neurons in this region do have an excitatory effect on secretion of ACTH.

Topics: 2-Amino-5-phosphonovalerate; Adrenocorticotropic Hormone; Animals; Cardiovascular System; Constriction, Pathologic; Hemorrhage; Hypercapnia; Hypoxia; Injections; Medulla Oblongata; Muscimol; Rabbits; Stimulation, Chemical; Vasopressins; Vena Cava, Inferior

The effect of CCK-8 (50 ng, i.c.v.) on the neurohypophysial vasopressin and oxytocin storage was estimated in haemorrhaged (1 ml per 100 g b.w.) male Wistar rats. In another experimental series rats dehydrated for three days were given CCK-8 in a daily i.c.v. dose of 50 ng. The neurohypophysial vasopressin and oxytocin content was bioassayed by pressor effect following Dekański or milk-ejection activity in vitro following van Dongen and Hays, respectively. The decrease of neurohypophysial vasopressin and oxytocin content, brought about by dehydration, was significantly less marked in animals treated with CCK-8. The depletion of neurohypophysial vasopressin and oxytocin content in haemorrhaged animals could be completely inhibited by earlier i.c.v. administration of CCK-8. It is suggested that hypothalamic cholecystokinin may serve as a modulator of neurohypophysial function.

Topics: Animals; Bloodletting; Dehydration; Disease Models, Animal; Hemorrhage; Injections, Intraventricular; Male; Models, Biological; Oxytocin; Pituitary Gland, Posterior; Rats; Rats, Wistar; Sincalide; Vasopressins

Intracerebroventricular hANP (50 nmol) inhibits release of vasopressin and oxytocin following dehydration as well as after haemorrhage. 10 nmol/L hANP markedly inhibits vasopressin and oxytocin release in vitro from the neurointermediate lobes both under basal condition as well as during stimulation with excess (56 mM) potassium. It is suggested that ANP may serve as a modulator of vasopressin and oxytocin release. The respective processes are localized, at least in part, at the neurohypophysial level.

Topics: Animals; Atrial Natriuretic Factor; Dehydration; Femoral Vein; Hemorrhage; Injections, Intraventricular; Male; Oxytocin; Pituitary Gland, Posterior; Pituitary Hormones, Posterior; Potassium; Rats; Rats, Wistar; Vasopressins

Postoperative bleeding from a stapled intestinal anastomosis is a rare complication. In previously reported cases, the bleeding either ceased spontaneously or required reoperation for direct control. We report two cases in which the bleeding was controlled using an intra-arterial vasopressin infusion. To our knowledge, this technique has not been previously reported for management of this problem. We had initial concerns about creating ischemia at the anastomosis, which could lead to disruption. Neither patient demonstrated subsequent problems with the anastomosis. Intra-arterial vasopressin infusion appears to be an effective method for controlling bleeding from a stapled intestinal anastomosis and can avert the need for reoperation.

Topics: Aged; Anastomosis, Surgical; Hemorrhage; Humans; Infusions, Intra-Arterial; Intestines; Male; Middle Aged; Retroperitoneal Neoplasms; Sigmoid Neoplasms; Surgical Staplers; Vasopressins

The effect of elevated cerebrospinal fluid Na+ concentration (CSF [Na+]) on the tolerance of blood loss, and concomitant cardiovascular and humoral responses were studied in conscious sheep. A slow (0.7 ml kg-1 min-1) venous haemorrhage was continued until the mean systemic arterial pressure suddenly decreased to less than 50 mmHg, or in the absence of hypotension, until a total blood loss of 25 ml kg-1. Significantly more blood had to be removed to induce hypotension in animals receiving an intracerebroventricular (i.c.v.) infusion (0.02 ml min-1) of 0.5 M NaCl (starting 30 min before haemorrhage and continued throughout the experiment) compared to control haemorrhages without concomitant i.c.v. infusion (22.7 +/- 1.2 ml vs 16.9 +/- 0.9 ml kg-1). In one animal, subjected to 0.5 M NaCl infusion, the blood pressure was still maintained at 25 ml kg-1 of haemorrhage. In spite of a larger blood loss, animals receiving i.c.v. infusion of hypertonic NaCl had an improved recovery of the blood pressure after haemorrhage, due to a better maintained cardiac output rather than to a reinforced increase of the vascular resistance. The improved cardiovascular responses to haemorrhage during elevated CSF [Na+] are not readily explained by the effects on the plasma concentrations of vasopressin, angiotensin II or noradrenaline, although the latter was augmented. The plasma protein concentration decreased already during the 30 min of hypertonic NaCl infusion preceding haemorrhage, and the haemodilution caused by the subsequent blood removal was aggravated, which indicates that this treatment also causes transfer of fluid to the plasma compartment. We conclude that elevated CSF [Na+] increases tolerance to haemorrhage and improves cardiovascular function after blood loss in sheep. Since the haemodynamic responses in many respects were similar to those reported in response to the systemic administration of a small volume of hypertonic NaCl solution in haemorrhagic shock, part of the effect of that treatment may be mediated via cerebral effects of increased Na+ concentration.

Topics: Angiotensin II; Animals; Female; Hemodynamics; Hemorrhage; Hypotension; Injections, Intraventricular; Norepinephrine; Saline Solution, Hypertonic; Sheep; Shock, Hemorrhagic; Vasopressins

Topics: Hemodynamics; Hemorrhage; Humans; Male; Middle Aged; Postoperative Complications; Shock, Septic; Vasopressins

1. The aim of the present study was to determine the effect of water restriction and/or hypoxia on the vasopressin response to haemorrhage in conscious rats. 2. Male, Long-Evans rats (n = 39) were prepared with chronically indwelling femoral artery and vein catheters and exposed to 24 h of one of the following: normoxia with ad lib drinking water (N + W); normoxia with water restriction (N - W); hypoxia with ad lib drinking water (H + W); and hypoxia with water restriction (H - W). At the end of 24 h, a 15 mL/kg arterial haemorrhage was performed. 3. Water restricted rats had elevated pre-haemorrhage vasopressin levels. Haemorrhage induced an increase in vasopressin in all groups. Water restriction (N - W) or hypoxia (H + W) each augmented the vasopressin response to haemorrhage. However, the combination of hypoxia and water restriction (H - W) failed to augment the vasopressin response to haemorrhage as compared to normoxic, water replete (N + W) rats. 4. Hypoxia or water restriction per se augment the vasopressin response to haemorrhage. This augmented vasopressin response to haemorrhage is not maintained when hypoxia and water restriction are combined.

Topics: Animals; Blood Pressure; Hemorrhage; Hypoxia; Male; Rats; Rats, Inbred Strains; Vasopressins; Water Deprivation

Hemorrhage-induced changes in the plasma vasopressin concentration and mean arterial blood pressure (MABP) were studied in conscious rats of both sexes with and without central alpha 1-adrenoreceptor blockade. Rats were subjected to two sequential hemorrhages (H1 and H2), each 0.8% of body weight after an intracerebroventricular injection of the alpha 1-adrenoreceptor antagonist corynanthine or of vehicle. H1 stimulated vasopressin secretion more in proestrous females than in males; there were no significant sex-related differences in responses to H2. Corynanthine pretreatment attenuated the vasopressin response to H2 in males, potentiated this response in proestrous females, but had no effect in estrous females. MABP decreased after H1 in all female groups and in corynanthine-pretreated males. After H2, all groups were hypotensive to the same extent. These data indicate that central alpha 1-adrenoreceptor-mediated pathways participate in vasopressin and blood pressure responses to hemorrhage, but their role is complex and is dependent on gender and on the phase of the estrous cycle.

Topics: Animals; Blood Pressure; Cerebral Ventricles; Estrus; Female; Hemorrhage; Injections, Intraventricular; Male; Phenylephrine; Proestrus; Rats; Rats, Inbred Strains; Receptors, Adrenergic, alpha; Sex Characteristics; Vasopressins; Yohimbine

Measurements of arterial pressure, heart rate, and plasma vasopressin were obtained in unanesthetized late-pregnant rats after administration of human relaxin (hRlx) alone or in conjunction with hemorrhage. Forty-two timed-pregnant rats were prepared with chronic femoral cannulas on the 17th day of pregnancy for measurements on the 19th day. In three separate sets of experiments, mean arterial pressure and heart rate were measured for 10 min before administration of 2 mg/kg hRlx, 100 micrograms/kg hRlx, or vehicle and for 20 h thereafter; plasma vasopressin was determined 20 min before and 3 min after administration of hRlx or vehicle and 20 min after performing a 15-ml/kg 3-min hemorrhage. Neither mean arterial pressure nor heart rate was significantly different among rats administered 2 mg/kg hRlx, 100 micrograms/kg hRlx, or vehicle. Plasma vasopressin was not significantly different among rats administered 2 mg/kg hRlx, 100 micrograms/kg hRlx, or vehicle. The decreases and subsequent compensatory changes in mean arterial pressure and heart rate after hemorrhage and the increases in plasma vasopressin were not significantly different among rats administered vehicle or hRlx.

Topics: Animals; Blood Pressure; Cardiovascular System; Female; Heart Rate; Hemorrhage; Humans; Pregnancy; Pregnancy, Animal; Rats; Rats, Inbred Strains; Relaxin; Vasopressins

In 17 women with refractory bleeding after myoma resection a dilute vasopressin pack was applied. Twenty units of vasopressin was diluted with 30 ml normal saline solution. A 1-inch new gauze pack was soaked in the dilute vasopressin and packed into the uteri of patients with bleeding from the beds of resected submucous myomas. The pack was left in place for no more than an hour. In none of the cases was there bleeding after the removal of the pack nor were there any side effects that could be attributed to the vasopressin.

Topics: Administration, Intravaginal; Adult; Female; Hemorrhage; Humans; Hysteroscopy; Middle Aged; Myoma; Postoperative Complications; Vasopressins

In order to investigate the physiological role of angiotensin II (ANG II) in the control of vasopressin (VP) secretion, the VP responses to hypotension induced by hemorrhage (20 ml/kg, n = 10) or nitroprusside infusion (1-10 micrograms/kg.min, n = 9) were studied with or without blockade of ANG II formation by the converting enzyme inhibitor captopril in conscious rabbits. Administration of captopril (5 mg/kg, iv) caused a small decrease in mean arterial pressure but did not enhance the hypotensive response to subsequent hemorrhage or nitroprusside infusion. The renin response to both stimuli was enhanced by captopril, whereas the increase in plasma ANG II concentration was attenuated. Plasma VP (PAVP) concentration increased during hemorrhage (2.0 +/- 0.2-113.6 +/- 47.7 pg/ml, P less than 0.01) and nitroprusside infusion (2.1 +/- 0.3-5.1 +/- 1.0 pg/ml, P less than 0.01). Captopril did not change basal plasma PAVP, nor did it attenuate the VP responses to hemorrhage or nitroprusside. Indeed, captopril tended to enhance the VP responses to hemorrhage (2.3 +/- 0.3-147.1 +/- 65.9 pg/ml) and nitroprusside infusion (1.9 +/- 0.2-15.4 +/- 6.0 pg/ml). The relationship between log PAVP and mean arterial pressure during hemorrhage and nitroprusside infusion in the presence of captopril was not different than in the absence of captopril. These results indicate that in conscious rabbits, the renin-angiotensin system does not contribute to the increase in VP secretion during hypotension induced by hemorrhage or nitroprusside infusion.

Topics: Angiotensin II; Animals; Blood Pressure; Captopril; Heart Rate; Hemorrhage; Hypotension; Male; Nitroprusside; Rabbits; Reference Values; Vasopressins

Extracellular norepinephrine (NE) levels in the paraventricular/anterior hypothalamic area (P/A) and in the dorsomedial medulla (DM) in conscious Sprague-Dawley rats were estimated by in vivo microdialysis before, during, and after sustained hypotension (75 mmHg mean arterial pressure) produced either by hemorrhage (Hem) or by 2-chloroadenosine infusion (2-Cl-ADO, 2.6-26.0 micrograms/min iv). P/A and DM NE were also measured before, during, and after hypertonic saline infusion (HTS; 1.5 M NaCl at 10 microliters.100 g-1.min-1 iv). P/A and DM NE increased during both Hem and 2-Cl-ADO and returned to baseline after reinfusion of hemorrhaged blood or after 2-Cl-ADO was stopped. However, Hem caused greater increases in P/A NE than 2-Cl-ADO despite equivalent decreases in blood pressure. Hem and 2-Cl-ADO produced equivalent changes in DM NE. HTS did not change P/A or DM NE despite increases in blood pressure of approximately 15 mmHg and plasma osmolality of approximately 30 mosmol/kgH2O. We conclude that 1) hypotension increases P/A and DM NE, which may mediate compensatory responses, 2) Hem is a more potent stimulus for NE release in the P/A than isovolemic hypotension induced by 2-Cl-ADO, and 3) the hypertensive response to HTS does not involve changes in P/A or DM NE.

Topics: 2-Chloroadenosine; Animals; Blood Pressure; Central Nervous System; Consciousness; Hemorrhage; Hypotension; Male; Medulla Oblongata; Norepinephrine; Osmolar Concentration; Paraventricular Hypothalamic Nucleus; Rats; Rats, Inbred Strains; Vasopressins

This study was designed to investigate whether an infusion of atrial peptide is capable of modulating the hormonal and hemodynamic responses elicited by acute hemorrhage. Conscious dogs were bled at a rate of 0.8 ml.kg-1.min-1 until 20 ml of blood/kg body wt had been removed. Two experiments were performed on each dog; in one experiment the animal was given alpha-human atrial natriuretic peptide (alpha-hANP) (50 ng.kg-1.min-1) dissolved in saline; in the other only the saline vehicle was given. Right and left atrial pressures decreased during hemorrhage in all experiments; the absolute decreases were greater when the animals received atriopeptin, but the differences between treatments were statistically significant only for right atrial pressure. Cardiac output decreased (P less than 0.05) and total peripheral resistance increased (P less than 0.05) during hemorrhage when atriopeptin was infused; although these variables showed similar trends when vehicle alone was infused during hemorrhage, no significant changes occurred. Infusion of atrial peptide did not affect the decrease in arterial blood pressure that occurred during hemorrhage. The increase in plasma vasopressin induced by hemorrhage was potentiated, but the increase in plasma renin activity was attenuated when alpha-hANP was infused. Hemorrhage increased circulating aldosterone levels in each experiment, but the response was less pronounced when alpha-hANP was given during the experiment. Intravenous administration of alpha-hANP modulates the hemodynamic responses elicited by hemorrhage, potentiates the rise in plasma vasopressin, and attenuates the rise in plasma renin activity induced by acute blood loss in conscious dogs.

Topics: Aldosterone; Animals; Atrial Natriuretic Factor; Blood Pressure; Cardiac Output; Dogs; Epinephrine; Female; Hematocrit; Hemorrhage; Osmolar Concentration; Potassium; Renin; Sodium; Vascular Resistance; Vasopressins

There is evidence for sex-related differences in the cardiovascular actions of vasopressin. Furthermore, receptors for the gonadal steroid hormones are located in centers in the brain involved in the control of vasopressin release and in cardiovascular regulation. We have, therefore, examined the effects of hemorrhage on mean arterial blood pressure, the plasma vasopressin concentration, and plasma renin concentration in conscious male and female rats. In preliminary experiments, no differences were found in blood and plasma volumes with respect to either sex or phase of the estrous cycle. In separate experiments, rats were subjected to two hemorrhages of 10% of blood volume, separated by an interval of 15 minutes. There were no substantial gender- or cycle-related differences in the ability of hemorrhaged rats to maintain mean arterial blood pressure or increase plasma renin concentration. The increase in plasma vasopressin concentration was greater in proestrous females than in males after the first hemorrhage and in diestrous, proestrous, and metestrous females than in males after the second hemorrhage. Pretreatment with a V1-receptor antagonist was without statistically significant effect on the mean arterial blood pressure responses in males, but it impaired blood pressure compensation in females. There are, then, gender- and cycle-related differences in vasopressin responses to hemorrhage, and vasopressin appears particularly important for blood pressure compensation to hemorrhage in female rats.

Topics: Animals; Blood Pressure; Blood Volume; Cardiovascular System; Estrus; Female; Heart Rate; Hemorrhage; Male; Rats; Rats, Inbred Strains; Receptors, Angiotensin; Receptors, Vasopressin; Sex Characteristics; Vasopressins

Previous studies have indicated that the area postrema (AP) of the rat is necessary for the development of chronic angiotensin-dependent hypertension. The present study assesses the role of the AP in the maintenance of arterial pressure during hemorrhage. Sprague-Dawley rats were given sham or AP lesions 1 wk before the experiment. They were instrumented with femoral arterial and venous catheters 2 days before the experiment. On the day of the experiment, base-line mean arterial pressure (MAP) was measured for 1 h before hemorrhage. During the following 45 min, each rat was subjected to one 7-ml/kg hemorrhage every 15 min for a total of three hemorrhages. MAP was monitored by computerized data acquisition. As shown previously, MAP was slightly but significantly lower in AP-lesion rats compared with sham-lesion rats before the hemorrhage procedure. In AP-lesion rats, hemorrhage resulted in a significantly greater fall in arterial pressure than in sham-lesion rats. In spite of larger drops in pressure in AP-lesion rats, hemorrhage caused equivalent increases in plasma renin and vasopressin in both groups. In AP-lesion rats compared with sham-lesion rats, significant bradycardia was present before hemorrhage. Hemorrhage caused bradycardia in both sham- and AP-lesion rats relative to the prehemorrhage heart rates, but AP-lesion rats showed greater bradycardia than did sham-lesion rats during every time period. We conclude that the AP may play an important role in the defense of arterial pressure against hemorrhage.

Topics: Animals; Blood Pressure; Blood Volume; Cerebral Ventricles; Hemorrhage; Male; Medulla Oblongata; Rats; Rats, Inbred Strains; Renin; Time Factors; Vasopressins

An extracorporeal circulation technique was developed for use in rats to provide equilibrated blood samples for multiple hormone assays. The inclusion of the extracorporeal circulation did not significantly alter arterial blood pressure, cardiac output, heart rate or central venous pressure in either Brattleboro rats with hereditary diabetes insipidus (BDI) or normal rats of the parent Long Evans (LE) strain. Plasma adrenaline and noradrenaline levels did not alter in either BDI or LE rats following inclusion of the extracorporeal circulation but the vasopressin concentration rose significantly in the LE rats. The impaired recovery of the mean arterial blood pressure following haemorrhage in the BDI rats compared with normal LE animals was not further influenced by the inclusion of the extracorporeal circulation. Plasma vasopressin and adrenaline (but not nor-adrenaline) levels were significantly raised during, and after, haemorrhage in the LE rats while in the BDI rats only plasma adrenaline levels were significantly increased. These results show that the insertion of an extracorporeal circulation into an anaesthetized BDI or LE rat does not adversely affect the cardiovascular system despite the increase in baseline plasma vasopressin concentration in normal rats, and its subsequent removal provides an additional equilibrated blood sample for multiple hormone assay within the same animal. The increased release of both adrenaline and vasopressin (but not noradrenaline) after haemorrhage in the same animal is detected using this technique, and the importance of vasopressin to the normal recovery process confirmed.

Topics: Anesthesia; Animals; Blood Pressure; Cardiac Output; Cardiovascular Physiological Phenomena; Catecholamines; Diabetes Mellitus, Experimental; Epinephrine; Extracorporeal Circulation; Heart Rate; Hemorrhage; Male; Norepinephrine; Rats; Rats, Inbred BB; Vasopressins; Venous Pressure

The interaction between vasopressinergic and prostanoid mechanisms in the control of cerebral hemodynamics in the conscious hypotensive newborn pig was investigated. Indomethacin treatment (5 mg/kg) of hypotensive piglets caused a significant decrease in blood flow to all brain regions within 20 min. This decrease in cerebral blood flow resulted from increased cerebral vascular resistances of 52 and 198% 20 and 40 min after treatment, respectively. Cerebral oxygen consumption was reduced from 2.58 +/- 0.32 ml.100 g-1.min-1 to 1.01 +/- 0.12 and 0.29 +/- 0.08 ml.100 g-1.min-1 20 and 40 min after indomethacin, respectively, in hemorrhaged piglets. Treatment with the putative vascular (V1) receptor antagonist [1-(beta-mercapto-beta, beta-cyclopentamethylene propionic acid-2-(O-methyl)tyrosine]arginine vasopressin (MEAVP) had no effect on regional cerebral blood flow, calculated cerebral vascular resistance, or cerebral metabolic rate either before or during hemorrhagic hypotension. However, decreases in cerebral blood flow and metabolic rate and increases in vascular resistance on treatment with indomethacin were blunted markedly in animals treated with MEAVP. These data are consistent with the hypothesis that the prostanoid system contributes to the maintenance of cerebral blood flow and cerebral metabolic rate during hypotension in the newborn pig, as reported previously, and implicate removal of vasopressinergic modulation by prostanoids as a potential mechanism for indomethacin-induced cerebral vasoconstriction in hypotensive newborn piglets.

Topics: Animals; Animals, Newborn; Arginine Vasopressin; Biomechanical Phenomena; Blood Pressure; Cardiac Output; Cerebrovascular Circulation; Hemorrhage; Hypotension; Indomethacin; Lypressin; Oxygen Consumption; Prostaglandins; Swine; Vascular Resistance; Vasopressins

The observation that electrical stimulation of the renal nerves increases vasopressin secretion raises the possibility that the renal nerves may participate in the control of vasopressin secretion. In the present investigation, the effects of renal denervation on the vasopressin response to two reflex stimuli (nitroprusside infusion and hemorrhage) and two osmotic stimuli (hypertonic saline infusion and water deprivation) were studied in conscious, chronically prepared rabbits. Nitroprusside infusion in 13 intact and 14 denervated rabbits caused similar decreases in mean arterial pressure (MAP) and the increase in plasma arginine vasopressin concentration (PAVP) in intact (2.6 +/- 0.3 to 5.8 +/- 0.9 pg/ml, P less than 0.01) and denervated (2.8 +/- 0.3 to 5.7 +/- 1.3 pg/ml, P less than 0.01) rabbits was not significantly different. Hemorrhage (20 ml/kg) in 15 intact and 14 denervated rabbits caused similar decreases in MAP. Again, the increase in PAVP from 2.7 +/- 0.3 to 159.0 +/- 37.1 pg/ml (P less than 0.01) in intact and from 5.0 +/- 1.7 to 115.4 +/- 45.6 pg/ml (P less than 0.01) in denervated rabbits was not significantly different, nor was the relationship between PAVP and MAP in the two groups. In seven intact rabbits, hypertonic saline infusion increased PAVP from 4.0 +/- 0.9 to 10.9 +/- 2.8 pg/ml (P less than 0.05). The change in six denervated rabbits was not significantly different, nor was the relationship between PAVP and plasma osmolality. During water deprivation (24 h) in six intact rabbits, PAVP increased from 4.0 +/- 0.7 to 6.9 +/- 0.6 pg/ml (P less than 0.05). Again, the increase in PAVP in six denervated rabbits was not significantly different from that in the intact rabbits. The change in MAP during water deprivation in the two groups was also not significantly different. Renal cortical norepinephrine concentration in denervated kidneys was less than 10 ng/g wet wt. These results indicate that, in conscious rabbits, renal denervation does not impair the osmotic or reflex regulation of vasopressin secretion, nor does it interfere with blood pressure regulation during hypovolemia or hypotension.

Topics: Animals; Blood Pressure; Denervation; Hemorrhage; Infusions, Intravenous; Kidney; Kidney Cortex; Male; Nervous System Physiological Phenomena; Nitroprusside; Norepinephrine; Osmolar Concentration; Rabbits; Saline Solution, Hypertonic; Vasopressins; Water Deprivation

Acute blood loss (16 ml/kg b. wt.) in conscious rats caused, 5 min later, increases in plasma vasopressin (AVP) concentration accompanied by reductions in arterial pressure and hematocrit. The plasma AVP response was markedly enhanced by intracerebroventricular injection (10 microliters) of a dopamine antagonist, haloperidol (0.15 mumol), which did not affect the responses of arterial pressure and hematocrit significantly. These results suggest that periventricular dopaminergic mechanisms may act to inhibit hemorrhage-induced AVP secretion.

Topics: Animals; Blood Pressure; Dopamine; Haloperidol; Hemorrhage; Injections, Intraventricular; Male; Paraventricular Hypothalamic Nucleus; Rats; Rats, Inbred Strains; Vasopressins

Denervation of sinoaortic baroreceptors in normovolemic rats selectively increases glucose utilization in the median eminence and pituitary neural lobe and enhances secretion of vasopressin and oxytocin. Hemorrhage in denervated animals increases further glucose metabolism in these structures and stimulates the release of both neurohypophysial hormones with preferentially a greater effect on vasopressin. Similar increases in glucose metabolism in these structures with a greater release of vasopressin are observed in sham-operated animals during hemorrhage. Absence of high-pressure receptors, therefore, does not modify the preferential release of vasopressin during hypovolemia. Hemorrhage also increases glucose utilization in the paraventricular and supraoptic nuclei, area postrema, and subfornical organ in sham-operated and denervated rats but only after a 20% blood reduction. The results indicate that decreased inputs from low-pressure receptors during hemorrhage increase the activity of the hypothalamoneurohypophysial system after small reductions in blood volume and that the activity of this system is tonically inhibited by baroreceptors. The activities of structures responsive to circulating angiotensin II (subfornical organ and area postrema) are stimulated by larger reductions in blood volume and their metabolic activities are not tonically influenced by high-pressure receptors.

Topics: Animals; Autoradiography; Brain; Denervation; Glucose; Hemorrhage; Male; Oxytocin; Pressoreceptors; Rats; Rats, Inbred Strains; Sinus of Valsalva; Vasopressins

The influence of aortic baroreceptors and vagal afferent nerves on the release of immunoreactive vasopressin (iVP) and immunoreactive atrial natriuretic factor (iANF) was examined in anaesthetized rabbits. Changes in plasma concentrations of iVP and iANF, heart rate, mean arterial pressure, and right atrial pressure were measured in response to blood volume changes (+20, +10, -10, -20%). Carotid sinus pressure was maintained at 100 mmHg (1 mmHg = 133.3 Pa), and blood volume changes were performed before and after bilateral vagotomy (VNX) in all experiments. Two experimental groups were studied: rabbits with aortic depressor nerves intact (ADNI) and those with aortic depressor nerves sectioned (ADNX). Mean arterial and right atrial pressures decreased during haemorrhage and increased in response to volume expansion. Plasma iVP concentrations increased with haemorrhage and decreased with volume expansion in the ADNI group. Plasma iANF, however, decreased with haemorrhage and increased during volume expansion in both ADNI and ADNX groups. Vagotomy caused an increase in baseline plasma iANF in the ADNX group. The responses of iANF to blood volume changes were augmented after VNX and ADNX. The results show that neither the aortic baroreceptor nor the vagal afferent input are needed for the iANF response to changes in blood volume, over the range of +/- 20%. In contrast, intact aortic baroreceptors are essential for changes in circulating iVP in this preparation.

Topics: Animals; Aorta; Atrial Natriuretic Factor; Blood Pressure; Blood Volume; Hemorrhage; Rabbits; Radioimmunoassay; Reference Values; Vasopressins

Hemorrhage stimulates endocrine and cardiovascular reflex responses that are appropriate for returning blood volume and pressure to prehemorrhage levels. Fetal sheep respond to hemorrhage with increases in plasma adrenocorticotropic hormone (ACTH), cortisol, and vasopressin concentrations and plasma renin activity, but little is known about the afferent limb of the reflex(es) controlling these responses. Fetal sheep between 128 and 133 days' gestation were chronically prepared with vascular catheters. Five fetal sheep were subjected to bilateral section of the cervical vagosympathetic trunks; six fetal sheep were not vagotomized. Four to six days after surgery, the fetuses were subjected to withdrawal of 10 ml of blood every 10 minutes for 2 hours (130 ml total). Vagotomized fetal sheep responded to the hemorrhage with a greater decrease in central venous pressure than the intact fetuses and a slower restitution of fluid to the vascular space (estimated to be 17% of the hemorrhage volume in 2 hours) than the intact fetuses (estimated to be 28% of the hemorrhage volume in 2 hours). Both groups of fetuses, however, responded to the hemorrhage with increases in fetal plasma ACTH, cortisol, and vasopressin concentrations and plasma renin activity that were not significantly different. A posteriori analysis of the data by correlation analysis revealed that the fetal ACTH, vasopressin, and renin responses to the hemorrhage were more highly correlated to the changes in fetal arterial pH than to changes in fetal mean arterial pressure or central venous pressure. The results suggest that the ACTH, vasopressin, and renin responses to hemorrhage in the fetus be mediated by chemoreceptors, not by cardiovascular mechanoreceptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adrenocorticotropic Hormone; Animals; Female; Fetus; Hemodynamics; Hemorrhage; Hydrogen-Ion Concentration; Nerve Fibers; Pregnancy; Renin; Sheep; Sympathetic Nervous System; Time Factors; Twins; Vagotomy; Vagus Nerve; Vasopressins

1. The changes in plasma concentrations of immunoreactive vasopressin (iVP) and atrial natriuretic factor (iANF) in response to haemorrhage (10-30% blood volume) were measured in 10 anaesthetized rabbits before and after cardiac receptor denervation (vagal nerve section). Carotid sinus pressure was maintained constant (60 mmHg) to eliminate any changing input from carotid baroreceptors. 2. Haemorrhage increased iVP before and after vagal nerve section indicating that withdrawal of input from aortic baroreceptors may have contributed to the increase in iVP. 3. Section of the vagus nerves attenuated the iVP response to haemorrhage. 4. There was no correlation between release of iVP and iANF. 5. Haemorrhage decreased iAF before and after vagal nerve section. Section of the vagus nerves increased iANF. Plasma iANF was highly correlated with atrial pressure and mean arterial pressure suggesting iANF release was secondary to changes in cardiac haemodynamics.

Topics: Animals; Aorta, Thoracic; Atrial Natriuretic Factor; Blood Pressure; Blood Volume; Heart Rate; Hemorrhage; Male; Myocardium; Rabbits; Radioimmunoassay; Receptors, Cell Surface; Time Factors; Vasopressins

Excision and skin grafting is the best treatment for burn wounds. In order to avoid excessive bleeding during the operation, sub-eschar infiltration with POR 8 (para ornithine 8 - vasopressin) has been performed in 115 patients between 1979 and 1984. The results being encouraging, infiltration was later also performed under the donor site. Bleeding was reduced enough by this technique to allow one stage excision and grafting of surfaces up to 20% of the body surface. No general or local complication of POR 8 infiltrations has been observed except a slight increase of blood pressure without clinical consequence.

Topics: Adolescent; Burns; Child; Child, Preschool; Hemorrhage; Humans; Infant; Ornipressin; Skin Transplantation; Vasopressins

Four physiological mechanisms are known to be important for recovery of arterial pressure (AP) after acute hemorrhage. These are the sino-aortic baroreflex (SA), the vagally mediated cardiopulmonary baroreflex (CP), the renin-angiotensin system (RA), and the vasopressin system (VP). We evaluated in anesthetized rabbits the relative importance of these mechanisms by repeating rapid, 10% arterial hemorrhage (6.5 ml/kg) once before and once after eliminating one of them and comparing the posthemorrhage hypotension. The study was conducted in two series. In the first series, we randomly grouped 24 rabbits into four groups, i.e., a sinoaortic baroreceptor-denervated group (SA) a vagotomized group (CP), a renin-angiotensin-blocked group (RA), and a vasopressin-blocked group (VP). In control conditions, AP fell to 88% at 2 min and 92% at 6 min after completing the hemorrhage. Significantly greater hypotension (e.g., 74% at 6 min) occurred only in the SA group. In the second series, we randomly classified 18 rabbits into three groups, i.e., an autonomic ganglion-blocked group (AB) plus a RA group and a VP group as before. Hypotension significantly greater than control (68% opposed to 91% at 6 min) occurred only in the AB group. We submit that as far as restoration of arterial pressure after rapid, mild hemorrhage in the rabbit is concerned, the arterial baroreceptor reflex system plays a far more important role than the vagally mediated cardiopulmonary baroreflex, the vasopressin system, or the renin-angiotensin system triggered directly by a fall in renal arterial pressure.

Topics: Animals; Autonomic Nerve Block; Heart Rate; Hemorrhage; Hypertension; Pressoreceptors; Rabbits; Reflex; Renin-Angiotensin System; Vagotomy; Vasopressins

The present study examined the effects of central and peripheral administration of a vascular (V1) vasopressin (AVP) receptor antagonist on blood pressure, heart rate, and AVP levels in conscious rats. Rats subjected to rapid arterial haemorrhage were administered the AVP V1 antagonist [d(CH2)5Tyr(Me)AVP] either 5 min pre- or 20 min posthaemorrhage. Mean arterial blood pressure (MAP) was monitored for 45 min, after which the animals were killed and selected brain regions and plasma taken for AVP measurement. Intravenous (i.v.) administration of d(CH2)5Tyr(Me)AVP at 10 micrograms kg-1, but not 100 ng kg-1, significantly reduced MAP between 20 and 45 min posthaemorrhage compared with saline-treated controls. In contrast, administration of d(CH2)5Tyr(Me)AVP at 100 ng kg-1 intracerebroventricularly caused an attenuated MAP recovery to haemorrhage comparable with the effect of the antagonist at 10 micrograms kg-1 i.v. Haemorrhage caused a marked increase in circulating AVP levels, which was further enhanced in rats treated with the V1 antagonist at 10 micrograms kg-1 i.v., but no change in AVP levels of selected brain regions. The results indicate a role for AVP in MAP recovery following haemorrhage which may be centrally mediated.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Brain; Chromatography, High Pressure Liquid; Female; Heart Rate; Hemodynamics; Hemorrhage; Hypothalamus; Injections, Intravenous; Injections, Intraventricular; Radioimmunoassay; Rats; Vasopressins

To determine the importance of alpha 1-adrenergic receptors in the endocrine responses of fetal lambs to hemorrhage, eight chronically instrumented fetal lambs were bled of 20% of their measured blood volume after pretreatment with prazosin (24.8 +/- 2.1 days' gestation) or inert vehicle (124.2 +/- 2.2 days' gestation) according to a randomized, crossover protocol. Cortisol levels increased threefold with prazosin injection and remained elevated after hemorrhage but did not change with hemorrhage after vehicle infusion. Plasma renin activity was unaffected by the injection of prazosin but increased in both groups after hemorrhage. Vasopressin levels were unchanged in the control group throughout the experiment but increased tenfold with hemorrhage after pretreatment with prazosin. alpha 1-Adrenergic receptor blockade removes adrenergic inhibition of cortisol secretion and changes the hypotensive threshold for the secretion of vasopressin.

Topics: Adrenergic alpha-Antagonists; Animals; Endocrine Glands; Hemodynamics; Hemorrhage; Hydrocortisone; Prazosin; Renin; Sheep; Vasopressins

An increase in atrial pressure has been shown to cause an increase in the concentration of atrial peptides (atriopeptin) in plasma. We therefore hypothesized that a reduction in atrial pressure would decrease the concentration of atriopeptin in plasma. In formulating this hypothesis we assumed that changes in the concentration of other circulating hormones or changes in cardiac nerve activity during hemorrhage would not affect the secretion of atriopeptin. To test the hypothesis, we bled sham-operated conscious dogs at a rate of 0.8 ml.kg-1.min-1 to decrease right and left atrial pressures. Hemorrhage was continued until a total of 30 ml of blood per kilogram body weight had been removed. Identical experiments were performed on conscious cardiac-denervated dogs. The concentration of plasma atriopeptin was decreased in each group of dogs after 10 ml of blood per kilogram of body weight had been removed, but the decrease achieved statistical significance only in the cardiac-denervated dogs. Further hemorrhage, however, produced no further decreases in circulating atriopeptin in either group even though atrial pressures continued to decline as more blood was removed. A comparison of the atriopeptin response to hemorrhage revealed no significant difference between the sham-operated and cardiac-denervated dogs, thus providing no evidence for a specific effect of cardiac nerves on atriopeptin secretion during hemorrhage. Our results demonstrate that the relationship between atrial pressure and plasma atriopeptin that has been observed repeatedly during atrial stretch is not evident during relatively slow, prolonged hemorrhage. There is, however, a small decline in circulating atriopeptin during the initial stage of hemorrhage that could be of biological significance.

Topics: Animals; Atrial Natriuretic Factor; Dogs; Female; Hematocrit; Hemodynamics; Hemorrhage; Osmolar Concentration; Potassium; Time Factors; Vasopressins

Vasopressin was used in ten critically ill patients with massive intra-abdominal bleeding unresponsive to conventional therapy. Vasopressin controlled bleeding in four patients, three of whom had continued to bleed following laparotomy for haemostasis; in two other patients, bleeding was reduced. All the patients were intensively monitored throughout the period of the vasopressin treatment; this enabled other physiological effects of vasopressin to be documented and reported. Mean arterial pressure and central venous pressure increased following the administration of vasopressin and there was a decrease in heart rate. Core body temperature rose significantly. Although all the patients had impaired renal function before receiving vasopressin, five had a prompt diuresis following its administration. Eight patients died but only three of intra-abdominal bleeding; two patients survived to leave hospital. Four patients had post-mortem evidence of ischaemia in the heart, liver and gastrointestinal tract; vasopressin may have contributed to the development of this. Vasopressin may have a place in the management of patients with life-threatening intra-abdominal haemorrhage but its use should be confined to those patients in whom conventional therapy has failed.

Topics: Abdomen; Adolescent; Adult; Female; Hemorrhage; Humans; Liver Transplantation; Male; Middle Aged; Postoperative Complications; Time Factors; Vasopressins

The effect of haemorrhage on plasma potassium concentration was studied in Sprague-Dawley rats, Brattleboro (BDI) rats and the parent strain Long-Evans (LE) rats. Haemorrhage induced an increase in plasma potassium within 10 min in all rats studied; 20 and 30 min later, plasma potassium was back to prehaemorrhage level. Changes in plasma sodium concentration were not statistically significant. When haemorrhage (1.0% of body weight) was repeated in the same animal preparation, there was a further significant increase in plasma potassium, but a fall in plasma sodium concentration. When vasopressin was injected intravenously, plasma potassium concentration did not change significantly (-0.21 +/- 0.21 mmol/l) in LE rats, whilst it increased significantly (0.69 +/- 0.20 mmol/l, p less than 0.001; paired t-test) in the BDI rats. The results suggest that haemorrhage-induced hyperkalaemia is unrelated to vasopressin, despite the fact that it increases plasma potassium concentration in the BDI rats when injected.

Topics: Animals; Hemodynamics; Hemorrhage; Hyperkalemia; Male; Potassium; Rats; Rats, Brattleboro; Rats, Inbred Strains; Sodium; Species Specificity; Vasopressins

These experiments were designed to investigate whether a reflex arising from ventricular receptors is capable of stimulating vasopressin secretion during hemorrhage. Three groups of conscious dogs (sham operated, cardiac denervated, and ventricular denervated) were hemorrhaged slowly until 30 ml blood/kg body wt had been removed. Hemorrhage produced comparable decreases in stroke volume, central venous pressure, and left atrial pressure in each group of dogs but produced a different pattern of heart rate response in each group. Plasma vasopressin concentrations before hemorrhage did not differ in the three groups of dogs. In sham-operated dogs plasma vasopressin increased from a control level of 2.4 +/- 0.3 to 6.2 +/- 1.7, 200.0 +/- 65.4, and 991.3 +/- 220.9 pg/ml after 10, 20, and 30 ml/kg of blood had been removed, respectively. In contrast, plasma vasopressin did not increase in either cardiac-denervated or ventricular-denervated dogs after 10 ml/kg of blood had been removed, and the increases in circulating vasopressin after 20 and 30 ml/kg hemorrhage were markedly attenuated by cardiac denervation and by ventricular denervation. The magnitude of the increase in plasma vasopressin in the cardiac-denervated and ventricular-denervated dogs did not differ significantly at comparable levels of hemorrhage. The results are consistent with the possibility that a reflex initiated by ventricular receptors is primarily responsible for stimulating the secretion of vasopressin during hemorrhage in conscious dogs.

Topics: Aldosterone; Animals; Dogs; Female; Heart; Heart Conduction System; Heart Rate; Hemorrhage; Natriuresis; Reference Values; Reflex; Renin; Vasopressins

Topics: Animals; Atrial Natriuretic Factor; Blood Pressure; Female; Goats; Heart Rate; Hemodynamics; Hemorrhage; Hypotension; Pregnancy; Pregnancy Complications, Cardiovascular; Respiration; Vasopressins

This study investigated whether excision of either the right or left atrial appendage of rats alters their natriuretic response and the release of atrial natriuretic factor during acute blood volume expansion or reduction. These animals were subjected to a thoracotomy and either had their right or left atrial appendages removed or underwent a right or left atrial sham appendectomy for comparative, control purposes. Intrajugular vein, intracarotid artery, and intravesical catheters were installed 3-4 weeks later under sodium pentobarbital anesthesia. Then, when the rats were conscious, blood volume was expanded using blood from donor rats once every 15 minutes in 3 increments of 10% of the calculated total blood volume at a rate of 5 ml/kg/min. Blood and urine samples were collected before volume expansion and at the end of each 15-minute period, with the withdrawn blood being replaced. A maximal fourfold increase in urinary volume, urinary sodium excretion, and plasma atrial natriuretic factor was observed in all but the right-atrial-appendectomized animals. Plasma atrial natriuretic factor, urinary volume, and urinary sodium excretion were correlated in all 4 groups. No significant changes in blood pressure or hematocrit were noted. Plasma vasopressin, measured at the end of volume expansion, was significantly lower in animals subjected to left atrial appendectomy. High-performance liquid chromatography of plasma from the control groups indicated that most of the released ANF during blood volume expansion corresponded to a high molecular weight peptide. Additional rats, processed as above, were subjected to 10% blood volume decrements.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Atrial Function; Atrial Natriuretic Factor; Blood Pressure; Blood Transfusion; Blood Volume; Disease Models, Animal; Heart Atria; Hemorrhage; Hypertension; Male; Natriuresis; Rats; Rats, Inbred Strains; Sodium; Urodynamics; Vasopressins

1. Plasma concentrations of atrial natriuretic peptide (ANP) and antidiuretic hormone (ADH) were measured in conscious stroke-prone spontaneously hypertensive (SPR), spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats before and after acute volume expansion or haemorrhage. 2. Plasma ANP concentration was reduced to one-third of resting values 30 min after a 1.5% haemorrhage (1.5 ml of blood per 100 g bodyweight). Plasma ADH concentration rose immediately 50-fold on haemorrhage and remained elevated at 30 min. 3. Plasma ANP concentration increased 2.5-fold relative to resting values 1 min after infusion of 2.0 ml per 100 g 5% dextrose; after 10 min plasma ANP remained elevated. Plasma ADH concentration tended to fall on volume expansion although no significant decrease was observed. 4. There was no difference in the basal levels of ANP and ADH, or in the changes produced by alterations in blood volume, in hypertensive SPR and SHR compared with normotensive WKY. 5. Thus, plasma ANP concentrations moved in opposite directions in response to two physiological stimuli: volume expansion and haemorrhage. Reciprocal changes were observed in plasma ADH.

Topics: Animals; Atrial Natriuretic Factor; Blood Volume; Hemorrhage; Hypertension; Male; Rats; Rats, Inbred SHR; Rats, Inbred Strains; Rats, Inbred WKY; Vasopressins

We studied the role of arterial and cardiac baroreceptors on mean arterial pressure (MAP) and release of arginine vasopressin (AVP) and plasma renin activity (PRA) during hemorrhage in conscious rabbits. Each rabbit was bled at 2% of its blood volume (BV) per minute until 35% had been removed, after which the blood was reinfused. Each rabbit was studied on three occasions, 7 days apart, and in each experiment, BV-MAP and BV-hormone response curves were constructed. The response to hemorrhage was examined when the input from arterial and cardiac baroreceptors were both intact; arterial baroreceptors only were intact (cardiac receptors were blocked with intrapericardial procaine); cardiac receptors only were intact (after sinoaortic denervation); neither receptor was intact. Resting AVP and PRA levels were unaffected by the various deafferentation procedures. AVP steeply increased only after more than 25% BV had been removed; this response was entirely mediated by cardiac baroreceptors. Increases in PRA occurred at BV loss greater than 15% and were largely independent of baroreceptor input. Maintenance of MAP during hemorrhage was mostly due to drive from the arterial baroreceptors. Thus AVP secretion during hemorrhage contributes little to the maintenance of MAP, and the hypovolemic stimulus to AVP release comes entirely from the cardiac baroreceptors.

Topics: Animals; Arginine Vasopressin; Arteries; Blood Pressure; Blood Volume; Heart; Hematocrit; Hemorrhage; Osmolar Concentration; Pressoreceptors; Rabbits; Renin; Vasopressins

This study was designed to evaluate the hemodynamic response to vasopressin infusion during hemorrhage and blood transfusion in a rat model of portal hypertension. Portal pressure, arterial pressure, and regional and systemic blood flows were measured in a rat model of portal hypertension receiving placebo or vasopressin infusion. Effects of the drugs were compared in control rats and rats subjected to hemorrhage and blood transfusion. In a stable portal hypertensive rat group (no hemorrhage or transfusion) a standard vasopressin dose, 2.5 mU X kg-1 X min-1, resulted in a significantly lower portal pressure (11.5 +/- 0.7 vs. 14.4 +/- 0.6 mmHg) with a concomitantly lower portal venous inflow (8.5 +/- 0.3 vs. 11.1 +/- 0.6 ml X min-1 X 100 g body wt-1) when compared with rats receiving placebo. These findings are in contrast to the effects obtained with the same dose of vasopressin given during blood transfusion to hemorrhaged portal hypertensive rats. The standard dose of vasopressin had no effect on any of the splanchnic or systemic circulatory parameters. Only when a dose of vasopressin 10 times larger was used in the hemorrhaged-transfused animals were hemodynamic effects noted. A significant decrease in portal flow and pressure was noted. These findings suggest that vasopressin given during hemorrhage may be less effective than when given during a stable state. Larger doses of vasopressin may be needed during hemorrhage to produce the same effect as seen during a controlled stable state. Caution should be used in extrapolating the results of pharmacologic studies in stable portal-hypertensive models to hypovolemic states in humans.

Topics: Animals; Blood Transfusion; Combined Modality Therapy; Disease Models, Animal; Drug Resistance; Hemodynamics; Hemorrhage; Hypertension, Portal; Male; Rats; Rats, Inbred Strains; Vasopressins

Overhydration inhibits release of vasopressin (VP) and oxytocin (OT) from the hypothalamo-neurohypophysial system during hypovolemia. We investigated whether opioid peptides mediate the inhibitory effect of water on secretion of these hormones. Conscious male rats were made hypovolemic by hemorrhage (HEM, 0.51 ml/min) of 20 and 35% of the blood volume or by injection of either subcutaneous polyethylene glycol (PEG, 20,000 mol wt, 35 ml/kg) or intraperitoneal histamine (HIS, 15 mg/kg, 1 ml/kg). Animals were intubated orally 1-4 min (HEM, HIS) or 6.75 h (PEG) later with or without administration of water (40 ml/kg). Four to seven min after intubation rats were injected with saline (1 ml/kg) or naloxone (2 or 5 mg/kg) and then decapitated 6-10 min later. Control animals were treated similarly but were not stimulated by hypovolemia. VP and OT were extracted from plasma and quantified by radioimmunoassay. Data were analyzed by analysis of variance. In HEM animals blood pressure fell and plasma osmolality increased, both of which correlated positively with the rise in plasma [VP] and [OT]. Overhydration lowered the plasma osmolality, attenuated the fall in blood pressure, and reduced [VP] and [OT] in plasma of HEM animals. The opiate receptor antagonist, naloxone, did not alter these changes in blood pressure or plasma osmolality, or the plasma [VP] after HEM in rats treated with or without water. Plasma [OT] was, however, increased by naloxone in both normally hydrated and overhydrated rats. Thus, regardless of the hydrational state of the animal, opioid peptides inhibited release of OT but not VP during hemorrhage. Data consistent with this interpretation were also obtained from rats made hypovolemic with PEG or HIS.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Blood Volume; Cardiovascular System; Endorphins; Hemorrhage; Histamine; Male; Naloxone; Osmolar Concentration; Oxytocin; Polyethylene Glycols; Rats; Rats, Inbred Strains; Vasopressins; Water

The possibility that neuropeptide Y (NPY) exerts organizational effects on central noradrenergic systems was investigated by treating newborn rats with subcutaneous injections of a specific NPY-antiserum. Three months later, neuroendocrine function was determined by measuring plasma vasopressin following haemorrhage, since this response is known to be regulated by ascending noradrenergic pathways. Basal mean arterial pressure, heart rate and plasma vasopressin were similar in both control (normal rabbit serum-treated) and NPY-antiserum-treated rats. Treatment with this antiserum resulted in an impaired vasopressin response to haemorrhage, although the haemodynamic changes observed after this hypovolaemic challenge were similar to control rats. NPY and noradrenaline content in the hypothalamus and brainstem were examined at the end of these experiments. NPY-like immunoreactivity was similar in both groups of animals. However, electrochemical detection of noradrenaline after HPLC revealed significantly higher levels in the hypothalamus, but not brainstem, of NPY-antiserum-treated rats. The presence of enduring changes in noradrenaline levels and neurohypophyseal function following neonatal treatment with NPY-antiserum suggests a role for NPY in postnatal organization of the rat hypothalamus.

Topics: Animals; Animals, Newborn; Blood Pressure; Brain Stem; Heart Rate; Hemorrhage; Hypothalamus; Immune Sera; Male; Neuropeptide Y; Norepinephrine; Rats; Rats, Inbred Strains; Vasopressins

The effects of continuous intravenous infusion of naloxone or vehicle on the blood pressure and vasopressin responses to step-wise hemorrhage were examined in conscious, age-matched spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto rats (WKY). Step-wise hemorrhage progressively lowered blood pressure and increased plasma vasopressin levels in both SHR and WKY. The WKY were relatively resistant to the hypotensive effect of hemorrhage. No significant differences were noted in blood pressure responses between naloxone-treated and vehicle-treated SHR while naloxone treatment attenuated hypotension only slightly in WKY. Plasma vasopressin levels were also elevated by naloxone treatment in SHR following a nonhypotensive hemorrhage equivalent to 0.5% of body weight. However, no differences were observed between plasma vasopressin levels in naloxone-treated and vehicle-treated SHR at greater degrees of hemorrhage. In addition, plasma vasopressin levels were similar at all times in hemorrhaged WKY, regardless of treatment. Plasma vasopressin levels were increased by naloxone in both time-control SHR and WKY. The data demonstrate that naloxone-sensitive systems exert only minimal effects on the immediate cardiovascular responses to hypovolemia in normotensive rats and no measurable effects in SHR. It does appear that naloxone-sensitive mechanisms contribute a small, but significant, tonic inhibitory influence over vasopressin secretion in both normotensive and hypertensive rats under basal conditions and in SHR in response to a small reduction in blood volume.

Topics: Animals; Blood; Blood Pressure; Heart Rate; Hemorrhage; Hypertension; Male; Naloxone; Osmolar Concentration; Rats; Rats, Inbred SHR; Rats, Inbred WKY; Receptors, Opioid; Vasopressins

The effect of haemorrhage on plasma lysine vasopressin concentrations and the cardiovascular effects of intravenous injections of synthetic lysine vasopressin were studied in twenty-four chronically catheterized pig fetuses aged between 81 and 114 d gestation (term = 114 +/- 1 d). Removal of 15-20% of the estimated blood volume reduced mean arterial blood pressure and elevated plasma vasopressin concentrations above the mean basal value of 2.2 +/- 0.3 muu./ml. The vasopressin concentration in plasma of fetuses younger than 104 d was insignificantly affected at 30 and 60 min after the bleed, whereas the corresponding values in older fetuses were raised by 12.7 +/- 7.2 muu./ml (d.f. = 7) and 16.0 +/- 6.0 muu./ml (d.f. = 7) respectively. The pituitary concentration of vasopressin was also greater towards the end of gestation. Plasma osmolality was unaffected by fetal blood loss. Maternal concentrations of vasopressin did not change from the basal values of 1.0 +/- 0.1 muu./ml (d.f. = 16). Injection of vasopressin raised fetal blood pressure and decreased heart rate. These results demonstrate that lysine vasopressin is present in the circulation of the pig fetus at 81 d (0.72 gestation), and that near term fetuses respond to haemorrhage more rapidly, and to a greater degree than younger fetuses.

Topics: Animals; Cardiovascular System; Female; Fetal Diseases; Hemorrhage; Injections; Lypressin; Pregnancy; Swine; Vasopressins

To assess the influence of vasopressin on splanchnic and renal circulatory changes induced by haemorrhage in portal hypertension, we studied 4 groups of 7 rats with chronic portal vein stenosis. Two groups received saline (C and H) and two groups vasopressin, 0.01 IU/kg/min (VP and VP-H). Ten minutes after starting drug infusion, group H and VP-H animals were allowed to bleed from the superior mesenteric vein. Both haemorrhage and vasopressin alone, decreased portal venous tributary blood flow and pressure but their association was not additive (as reflected by comparable bleeding rate in groups H and VP-H). By contrast, vasopressin increased renal perfusion in bleeding and non-bleeding animals whereas haemorrhage alone decreased renal perfusion. These results indicate that the effects of vasopressin on the splanchnic circulation in bleeding anaesthetized animals differ from the effects observed when blood volume is normal. Therefore, in patients with cirrhosis the effects of vasopressin during bleeding might also differ from those observed in patients in stable condition.

Topics: Anesthesia; Animals; Blood Pressure; Cardiac Output; Hemorrhage; Hypertension, Portal; Male; Rats; Rats, Inbred Strains; Renal Circulation; Splanchnic Circulation; Vascular Resistance; Vasopressins

In the paediatric burn unit of Brugmann University Hospital, children are treated conservatively for three weeks before excision and grafting. In order to avoid excessive bleeding during tangential excision of the granulating tissue, sub-eschar infiltration with Para-Ornithin-8-Vasopressin (POR 8), a synthetic neurohypophyseal-like hormone, has been performed since 1979 on 145 children. Bleeding is reduced dramatically by this technique. Therefore, since 1984, infiltration of the donor site with POR 8 was also performed in 25 children. Excision and grafting of areas up to 20% of total body surface are possible in one operation with a graft take rate of 95 to 100%. We didn't record any variation in heart rate. A 5 to 10% increase of arterial blood pressure occurred in all children. No general or local complications have been observed. We believe this technique to be of great help in the operative treatment of burns in children.

Topics: Adolescent; Burns; Child; Child, Preschool; Hemorrhage; Humans; Infant; Ornipressin; Prospective Studies; Retrospective Studies; Skin Transplantation; Vasopressins

The clearance of vasopressin (VP) by the kidneys and splanchnic viscera was studied in the anesthetized dog. VP is bound to plasma protein, 10% at basal plasma VP levels and 40% at plasma VP concentrations greater than 20 microU/ml. The urinary clearance of VP is 70-100% of the glomerular filtration rate; the renal organ clearance of the hormone is 20-30% greater than its urinary clearance. There is evidence that the renal organ clearance of VP is affected by changes in both glomerular filtration rate and renal blood flow. The renal clearance of VP is a result of glomerular filtration, degradation, or reabsorption in the proximal nephron, and secretion into the distal nephron. In the short term, the renal clearance of VP is unaffected either by changes in the plasma VP concentration over a broad range or by moderate hemorrhage. The splanchnic clearance of VP is accomplished almost equally by the intestine and the liver. Because the sum of the splanchnic and renal clearances of VP is less than estimates of its metabolic clearance rate, there may be a physiologically significant clearance of VP by organs in addition to the kidneys and splanchnic viscera.

Topics: Animals; Dogs; Glomerular Filtration Rate; Hemodynamics; Hemorrhage; Kidney; Liver; Pressure; Splanchnic Circulation; Ureter; Vasopressins

Vasopressin (VP) has been found in the cerebrospinal fluid (CSF) of several species of animals. Although it is known that hemorrhage, hypertonicity of body fluid, hypoxia, and hypercapnia all increase VP in plasma, little is known regarding the stimuli that cause the secretion of VP into the CSF. We therefore performed several studies to examine whether stimuli capable of increasing plasma levels of VP can also increase VP in the CSF of anesthetized dogs. We found that hemorrhage, intracerebroventricular infusion of hypertonic artificial CSF, hypoxia, and hypercapnia all produced increases in the concentration of VP in plasma and in CSF, but the time courses and the magnitude of the increases in the two compartments were different. In addition, an i.v. infusion of hypertonic saline or of hydrochloric acid produced an increase in plasma VP without significantly changing CSF VP. Thus, although the secretion of VP into plasma and CSF may be influenced by the same stimuli, changes in one compartment do not necessarily correlate with changes in the other. Taken together, our results are consistent with the hypothesis that the plasma and CSF VP may derive from different sources.

Topics: Acidosis; Animals; Cerebrospinal Fluid; Dogs; Hemorrhage; Hypercapnia; Hypoxia; Infusions, Parenteral; Injections, Intraventricular; Saline Solution, Hypertonic; Vasopressins

The responses of vasopressinergic neurons to acute salt loading and to graded hemorrhage were studied in rats under conscious and anesthetized conditions. Chronically cannulated rats were used in this study so that pre- and postanesthetic conditions could be studied in the same animals. Anesthesia induced by a combination of ketamine hydrochloride and pentobarbital sodium (Nembutal) did not cause a release of vasopressin-associated neurophysin (VP-RNP). In response to infusion of 18% saline, animals in the anesthetized state had significantly greater increases in plasma osmolality (Posmol) and plasma sodium concentration than animals in the conscious state. However, the rate of increase in plasma VP-RNP concentration ([VP-RNP]) as well as the relationship between [VP-RNP] and Posmol were not significantly different for the two states. Graded hemorrhage caused similar rates of increase in [VP-RNP] for animals under conscious and anesthetized conditions. These data suggest that anesthesia induced by ketamine plus pentobarbital sodium does not change the responsiveness of vasopressinergic neurons to acute salt loading and to graded hemorrhage.

Topics: Anesthesia, General; Animals; Arginine Vasopressin; Blood Pressure; Consciousness; Drug Combinations; Hemorrhage; Ketamine; Male; Neurons; Neurophysins; Osmolar Concentration; Oxytocin; Pentobarbital; Protein Precursors; Rats; Rats, Inbred Strains; Sodium; Sodium Chloride; Vasopressins

The effect of bilateral lesions of the fastigial nucleus of the cerebellum on the release of vasopressin in response to a hypovolemic-hypotensive stimulus was examined in unanesthetized rats. Electrolytic lesions of the rostromedial fastigial nucleus decreased plasma vasopressin levels and attenuated the release of vasopressin in response to hemorrhage. These results suggest that the fastigial nucleus is involved in the regulation of vasopressin release to baroreceptor information and support a role of the fastigial nucleus in the response to hemorrhage.

Topics: Animals; Blood Pressure; Blood Volume; Cerebellar Nuclei; Heart Rate; Hemorrhage; Male; Rats; Rats, Inbred Strains; Vasoconstriction; Vasopressins

The effect of two consecutive hemorrhages, each 10% of blood volume, on plasma vasopressin concentrations was determined in conscious unilaterally nephrectomized Long-Evans rats made hypertensive by treatment for 3 wk with deoxycorticosterone (DOC) and substitution of 1% saline for drinking water (DOC-salt rats) or DOC alone (DOC rats) and in normotensive unilaterally nephrectomized rats drinking water (H2O rats) or saline (NaCl rats). In response to 20% hemorrhage, blood pressure decreased more (P less than 0.01) and plasma vasopressin increased less (P less than 0.01) in the DOC-salt rats than in the other groups. Under basal conditions, immunoreactive vasopressin was found in the platelets in NaCl, DOC, and DOC-salt rats (P less than 0.01) but not in H2O rats. Platelet vasopressin increased (P less than 0.05-0.01) in response to hemorrhage only in DOC-salt rats. In conclusion, the vasopressin response to hemorrhage in DOC-salt rats is impaired; platelet immunoreactive vasopressin is of little importance in normal rats but is increased by treatment with DOC and/or chronic salt loading; and platelet vasopressin increased in response to hemorrhage only in DOC-salt rats.

Topics: Animals; Blood Platelets; Blood Volume; Desoxycorticosterone; Hemorrhage; Hypertension; Male; Nephrectomy; Rats; Saline Solution, Hypertonic; Time Factors; Vasopressins

Infusion of oxytocin into one vertebral artery of anesthetized dogs did not alter plasma vasopressin concentration, blood pressure or heart rate. However, there was a significant (p less than 0.01) increase in plasma renin activity (PRA; delta = 7.6 +/- 2.3 ng/ml X h). A 35% hemorrhage caused blood pressure to fall by 9.4 +/- 4.0 mm Hg (p less than 0.01) and PRA to rise by 8.8 +/- 2.7 ng/ml X h (p less than 0.05). In 8 dogs that were subjected to a similar hemorrhage and that also received an intravertebral infusion of oxytocin, blood pressure was maintained and PRA increased by 14 +/- 4.3 ng/ml X h (p less than 0.05). Heart rate and plasma vasopressin responses were similar in both hemorrhage groups. The results indicate that oxytocin prevented the fall in blood pressure associated with a hemorrhage, possibly by increasing renin release.

Topics: Animals; Blood Pressure; Brain; Dogs; Heart Rate; Hemorrhage; Injections, Intra-Arterial; Male; Oxytocin; Pressoreceptors; Renin; Vascular Resistance; Vasopressins; Vertebral Artery

Increases in plasma vasopressin and renin activity that occur in response to haemorrhage have been attributed in part to reflex effects from cardiac receptors and sinoaortic baroreceptors, but the relative importance of these different receptors in causing humoral changes during haemorrhage in conscious dogs has not been reported. We investigated this question by hemorrhaging 6 sham-operated (SO), 6 cardiac-denervated (CD), 4 sinoaortic-denervated (SAD), and 4 combined sinoaortic and cardiac-denervated (SACD), conscious dogs. Blood was removed at a rate of 0.9 ml/kg X min. Plasma vasopressin and renin samples were taken during a control period and after 10, 20, and 30 ml/kg of blood had been removed. Results (mean +/- SE) are shown in the tables below. (table; see text) These experiments illustrate that: resting plasma levels of vasopressin and renin in conscious dogs are unaffected by the denervation procedures used in these experiments, the increase in plasma vasopressin that occurs during haemorrhage is mediated largely via cardiac receptors, with a considerably smaller contribution from the sinoaortic baroreceptors, during moderately severe haemorrhage (30 ml/kg) vasopressin secretion can be increased by a mechanism independent of sinoaortic and cardiac reflexes, the increase in plasma renin activity that occurs during haemorrhage is not dependent upon either cardiac or sinoaortic reflexes.

Topics: Animals; Blood; Blood Pressure; Cardiac Output; Denervation; Dogs; Heart; Heart Rate; Hemorrhage; Homeostasis; Osmolar Concentration; Pressoreceptors; Renin; Sinus of Valsalva; Sodium; Stroke Volume; Vasopressins

The effect of an acute arterial haemorrhage of 15 ml/kg body weight on renal and intrarenal blood flow (measured using radioactive microspheres) was determined in anaesthetized rats. In order to assess the role of vasopressin in mediating the observed changes, the response to haemorrhage of animals lacking the ability to synthesize vasopressin (Brattleboro rats) was compared with that of the parent strain (Long Evans rats). In addition, a group of Long Evans rats was treated with an antagonist of the vascular action of vasopressin before being bled. Thirty minutes after haemorrhage the mean arterial blood pressure of untreated Long Evans rats was significantly higher than that of Brattleboro or vasopressin antagonist-treated Long Evans rats. Following haemorrhage, total renal vascular resistance increased markedly in untreated Long Evans rats. In these animals there were substantial increases in calculated vascular resistance in both inner and outer halves of the renal cortex. In Brattleboro rats there was only a small increase in renal vascular resistance, confined to the outer cortex, whilst in vasopressin antagonist-treated Long Evans rats there was no significant change in the vascular resistance of either cortical region. It is concluded that much of the increase in renal vascular resistance which follows haemorrhage is due to vasopressin. This vasoconstrictor effect of the hormone, which contributes to its pressor action after haemorrhage, occurs in both the inner and outer regions of the renal cortex.

Topics: Animals; Blood Pressure; Hemodynamics; Hemorrhage; Kidney Cortex; Male; Rats; Rats, Brattleboro; Renal Circulation; Vascular Resistance; Vasopressins

Topics: Adult; Cervix Uteri; Drug Evaluation; Fasciotomy; Female; Hemorrhage; Hemostatics; Humans; Hysterectomy; Intraoperative Complications; Ornipressin; Solutions; Vasoconstrictor Agents; Vasopressins

The effects of hemorrhage on plasma vasopressin levels and blood pressure were examined in conscious, age-matched spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto (WKY) rats. Graded hemorrhage was produced by bleeding the rats at 10 min intervals over a total period of 65 min, to produce cumulative blood losses equivalent to 0.5, 1.0, 1.5, 2.0 and 3.0% of body weight in each animal. Hemorrhage progressively lowered blood pressure and increased plasma vasopressin levels in both SHR and WKY. At cumulative reductions in blood volume equivalent to 1.0 to 3.0% of body weight, there were greater reductions in arterial pressure and greater increases in plasma vasopressin concentrations in SHR than WKY. Basal blood volume in SHR was 10% lower than in WKY. In SHR, the greater vasopressin response to hemorrhage may have been due in part to the greater fall in arterial pressure. Although the lower blood volume may have contributed to the latter, derangements in baroreceptor function may also have been important.

Topics: Animals; Blood Pressure; Catheterization; Heart Rate; Hemorrhage; Male; Plasma Volume; Rats; Rats, Inbred Strains; Time Factors; Vasopressins

Persistent, severe renal hemorrhage resulted from a diagnostic renal biopsy in a 19-year-old woman with chronic renal insufficiency. Infusion of vasopressin into the renal artery through an angiographic catheter produced prompt resolution of bleeding. This method has distinct advantages over surgical intervention or transcatheter embolization in the control of traumatic renal hemorrhage.

Topics: Adult; Biopsy, Needle; Female; Hemorrhage; Humans; Infusions, Intra-Arterial; Kidney; Kidney Diseases; Radiography; Renal Artery; Vasopressins

This study was designed to determine if vascular dysfunction and enhanced norepinephrine sensitivity occurring in early experimental juvenile diabetes (S. M. Mueller, T. M. Mueller, and P. J. Ertel, 1982, Amer. J. Physiol. 243, H139-H144) persist, improve, or worsen in adulthood. Alloxan was administered to rats at 4 weeks of age and they were studied 14 weeks later. After Seconal anesthesia, the hindquarters of diabetic and control rats were perfused at a constant flow rate per 100 g through the abdominal aorta with oxygenated Tyrode solution containing dextran. Efflux was from the ligated and severed inferior vena cava. In order to test the effect of a strong sympathetic stimulus producing reflex peripheral vasoconstriction, the cephalad portions of the rats were rapidly hemorrhaged. The time to the maximal increase was significantly longer in the diabetics (122 +/- 6 sec, P less than 0.05) than in the controls (102 +/- 5 sec) and the increase in perfusion pressure was markedly less in the diabetics (D) (48 +/- 9 mm Hg, P less than 0.01) than in the age-matched controls (C) (88 +/- 10 mm Hg). The threshold to norepinephrine in the perfusate was determined. The threshold was significantly lower in D than in age-matched C [0.112 +/- 0.026 (P less than 0.05) vs 0.265 +/- 0.057 micrograms/ml, respectively]. The maximum vasoconstrictor capacity of the vasculature was tested with supramaximal doses of vasopressin and was significantly lower in D than in C [190 +/- 10 (P less than 0.001) vs 284 +/- 15 mm Hg, respectively]. These data suggest that both vasculopathy and enhanced norepinephrine sensitivity persist in chronic uncontrolled experimental diabetes mellitus. However, when the severity of the abnormalities was compared to early experimental diabetes mellitus, mild improvement had occurred--an apparent adaptation to the diabetic state as the animal grew.

Topics: Aging; Animals; Blood Glucose; Blood Pressure; Body Weight; Diabetes Mellitus, Experimental; Fatty Acids, Nonesterified; Hemorrhage; Male; Norepinephrine; Rats; Rats, Inbred Strains; Vascular Resistance; Vasoconstriction; Vasodilation; Vasopressins

Haemorrhages in the course of cirrhosis and portal hypertension are surgical emergencies. Nevertheless medical treatment may be necessary both to revive the patient and temporarily to check the haemorrhaging itself. Some views are presented on the use of drugs, both those already in clinical use and others at the experimental stage, which appear to be effective in the treatment of haemorrhaging in portal hypertension (Vasopressin, glypressin, prostaglandin, somatostatin, propranolol, cimetidine and ranitidine).

Topics: Cimetidine; Emergencies; Hemorrhage; Humans; Liver Cirrhosis; Lypressin; Propranolol; Prostaglandins; Ranitidine; Somatostatin; Terlipressin; Vasopressins

We demonstrated previously that cerebellectomy or ablation of the fastigial nuclei (FN) in the dog impairs markedly the restoration of blood pressure and increases the death rate after severe hypotension. Angiotensin (AII) and vasopressin (AVP) participate in the pressor response to hypotension, and plasma levels of both are increased by electrical stimulation of the FN. The present studies examined the importance of the FN in mediating the secretion of AII and AVP after hemorrhage to 50 mm Hg. Cerebellectomy reduced significantly both the rate of recovery and level of maintenance of blood pressure after hemorrhage. Blockade of conversion of AI of AII with captopril produced a similar deficit, and combination of both treatments produced a greater impairment than either alone. Treatment with an AVP antagonist decreased the level of maintenance of blood pressure but not be initial rate of recovery. The AVP antagonist in combination with cerebellectomy did not produce a greater deficit than cerebellectomy alone. This would suggest that although the cerebellum mediates some activation of the renin-angiotensin system during severe hypotension, it may mediate most of the AVP secretion under these conditions.

Topics: Angiotensin II; Animals; Blood Pressure; Cerebellum; Dogs; Female; Hemorrhage; Hypotension; Male; Vasopressins

In 8 chronically cannulated fetal lambs between 119 and 127 days gestation the resting plasma norepinephrine concentration was 528 +/- 77 pg X ml-1 and the resting plasma epinephrine concentration 159 +/- 42 pg X ml-1. Hemorrhage of 20% of estimated blood volume at 2% per min produced a 2.1-fold increase in plasma norepinephrine levels and a 3.4-fold increase in plasma epinephrine levels when the animals were pretreated with an injection of saline (1 ml). Plasma catecholamine levels returned toward control values following return of the shed blood. In contrast, hemorrhage of these animals following pretreatment with an antagonist of the pressor effect of vasopressin did not cause an increase in fetal plasma catecholamine levels. Thus, vasopressin may mediate the sympathetic responses to volume depletion in the fetus.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Epinephrine; Female; Fetal Diseases; Fetus; Hemorrhage; Norepinephrine; Pregnancy; Sheep; Vasopressins

To determine if the posterior pituitary hormone vasopressin is important for maintaining fetal cardiovascular homeostasis during hypovolemic stress, in seven chronically catheterized fetal lambs we induced hemorrhage of 20% of estimated blood volume in the presence and in the absence of a potent antagonist to the pressor effects of vasopressin. The study was a paired crossover design with at least 48 hours separating experiments in the same animal. Injection of the vasopressin antagonist did not alter basal fetal heart rate or arterial blood pressure, but hemorrhage of 2% of estimated fetal blood volume per minute for 10 minutes produced a greater fall in blood pressure (13 +/- 2 versus 10 +/- 2 torr, p less than 0.05) when the blocker was present than when it was absent. Arterial blood pressure remained below control levels longer following hemorrhage when the fetuses were pretreated with the antagonist (49.7 +/- 6 versus 26.6 +/- 6 minutes, p less than 0.01), and the integrated fall in arterial blood pressure with hemorrhage was greatest (283 +/- 53 versus 169 +/- 57 mm Hg . min p less than 0.01) when the blocker was used. The fall in heart rate following hemorrhage was similar with and without blocker pretreatment. These results indicate that vasopressin plays a physiologic role in blood pressure regulation in fetal lambs during periods of hypovolemia.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Cardiovascular System; Catheters, Indwelling; Female; Fetal Diseases; Fetus; Heart Rate; Hematocrit; Hemorrhage; Homeostasis; Hydrogen-Ion Concentration; Pregnancy; Sheep; Time Factors; Vasopressins

1. The effects of naloxone on blood pressure recovery after either rapid arterial haemorrhage or prolonged venous haemorrhage were studied in rats lacking vasopressin (Brattleboro strain) and in control (Long Evans) rats. 2. To produce similar reductions in blood pressure, less blood had to be taken from the Brattleboro rats than from the Long Evans rats. 3. After rapid arterial haemorrhage in the absence of naloxone, blood pressure recovery was slower in Brattleboro rats than in Long Evans rats. Naloxone did not affect the response to rapid arterial haemorrhage in Long Evans rats, but improved blood pressure recovery in Brattleboro rats; despite this improvement, the Brattleboro rats remained hypotensive at a time when the Long Evans rats were normotensive. These findings suggest that both the absence of vasopressin and a depressor action of beta-endorphins may contribute to the poor ability of Brattleboro rats to cope with rapid haemorrhage. 4. After prolonged venous haemorrhage in the absence of naloxone, there was no difference between the recovery of blood pressure in Brattleboro rats and Long Evans rats. Naloxone improved blood pressure recovery to a similar extent in both strains of rat. These findings suggest that the absence of vasopressin does not impair blood pressure recovery after prolonged haemorrhage.

Topics: Animals; Blood Pressure; Heart Rate; Hemorrhage; Male; Naloxone; Rats; Rats, Brattleboro; Sodium Chloride; Vasopressins

A study was undertaken to investigate the effects of moderate nonhypotensive hemorrhage on the renal organ and urinary clearances of vasopressin in anesthetized dogs. A nonhypotensive hemorrhage was conducted in nine dogs by withdrawal of 12 ml/kg arterial blood over 10 min. This reduction in blood volume increased the plasma vasopressin concentration from a prehemorrhage value of 4.3 +/- 0.5 to 12.5 +/- 3.4 microU/ml (P less than 0.01) in the 15-min period immediately after hemorrhage and to 8.1 +/- 1.4 microU/ml (P less than 0.01) in the 45- to 60-min period after hemorrhage. The increased plasma vasopressin concentration was not associated with changes in either plasma osmolality or mean arterial blood pressure. The urinary excretion of vasopressin increased significantly after hemorrhage (P less than 0.01, 0-15 min after hemorrhage; P less than 0.05, 45-60 min after hemorrhage) and correlated significantly with the plasma vasopressin concentration (r = 0.92; P less than 0.001). However, this moderate nonhypotensive hemorrhage did not change the renal vasopressin extraction ratio or the renal organ and urinary clearances of vasopressin from their prehemorrhage values of 0.27 +/- 0.02, 2.00 +/- 0.20 ml/min X kg, and 1.43 +/- 0.13 ml/min X kg, respectively. At no time were these values different from those in nine time control dogs. Thus, changes in the renal handling of vasopressin do not contribute to the increase in the plasma vasopressin concentration after moderate nonhypotensive hemorrhage.

Topics: Animals; Blood Pressure; Blood Volume; Dogs; Hemorrhage; Male; Osmolar Concentration; Renal Circulation; Vasopressins

The blood pressure, heart rate, ACTH, corticosteroid, vasopressin, and renin responses to rapid 15 ml/kg hemorrhage were measured in six conscious healthy dogs with chronically maintained femoral arterial catheters. The hemorrhage decreased the mean arterial blood pressure slightly (P less than 0.001), increased the heart rate (P less than 0.001), and increased arterial plasma levels of ACTH (P less than 0.01), corticosteroids (P less than 0.001), vasopressin (P less than 0.001), and renin activity (P less than 0.001). Overall and in the individual experiments, there appeared to be little correspondence between the ACTH and corticosteroid responses. In none of the experiments was there a clear rise in ACTH above control levels before the first rise in corticosteroids. To ascertain that adrenal secretion of corticosteroids was increased during 15 ml/kg hypovolemia, changes in the clearance and distribution volume of cortisol were estimated by counting tritium extracted from plasma of five dogs infused with [1,2-3H] cortisol to steady state levels before and during hypovolemia. The stimulus caused a 30% reduction from steady state levels of dichloromethane-extractable tritium counts (P less than 0.001). Combined with the observed increase in plasma corticosteroid levels, these results show that the increase in adrenal secretion of corticosteroids after hemorrhage was underestimated by measurement of changes in peripheral plasma levels. The hypothesis that hemorrhage results in an increase in adrenal sensitivity to ACTH is tested in the following paper.

Topics: Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Animals; Blood Pressure; Dogs; Female; Heart Rate; Hemorrhage; Hydrocortisone; Kinetics; Male; Renin; Vasopressins

Topics: Adrenal Cortex; Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Animals; Dexamethasone; Dogs; Hemorrhage; Hydrocortisone; Male; Metabolic Clearance Rate; Renin; Vasopressins

Topics: Animals; Blood Pressure; Diabetes Insipidus; Ethanol; Heart Rate; Hemorrhage; Rats; Rats, Brattleboro; Rats, Mutant Strains; Vasopressins

Topics: Angiotensin I; Angiotensin II; Animals; Brain; Female; Goats; Hemorrhage; Rana temporaria; Reflex; Renin-Angiotensin System; Thirst; Vasopressins; Water; Water-Electrolyte Balance

To determine if the subnormal blood pressure recovery after hemorrhage in Brattleboro rats is due to secondary abnormalities in the renin-angiotensin or sympathetic nervous systems, we measured the hemodynamic, catecholamine, and renin activity responses to moderate acute hemorrhage in anesthetized Brattleboro rats. Results were compared to responses in groups of animals matched for either age or weight. Blood pressure recovery was significantly blunted (P less than 0.01) in Brattleboro rats compared to that in either control group, but heart rate responses were similar. Basal plasma norepinephrine was significantly higher in Brattleboro rats than in controls (P less than 0.001), but the response to hemorrhage was not significantly different. Both plasma epinephrine levels and renin activity were significantly higher before hemorrhage and increased more after hemorrhage in vasopressin-deficient animals. Plasma vasopressin in controls increased approximately 10-fold, reaching levels of 790 +/- 140 pg/ml in age-matched controls and 425 +/- 60 pg/ml in weight-matched controls. Vasopressin levels in Brattleboro rats were undetectable both before and after hemorrhage. We conclude from these data that the subnormal blood pressure recovery observed in vasopressin-deficient rats is not due to secondary abnormalities of the renin-angiotensin or sympathetic nervous systems, but, instead, is related more directly to the vasopressin deficiency.

Topics: Animals; Blood Pressure; Heart Rate; Hemodynamics; Hemorrhage; Norepinephrine; Rats; Renin; Renin-Angiotensin System; Time Factors; Vasopressins

To analyze the relationship between the splanchnic and systemic effects of vasopressin and to measure its efficacy in lowering portal pressure relative to what can be accomplished by zero gradient shunting, intraoperative measurements of cardiac output and relevant pressures were made in 30 patients undergoing selective or total shunts. Vasopressin caused a significant increase in systemic vascular resistance and pulmonary capillary wedge pressure, but an insignificant overall reduction in cardiac index (CI). However, in ten patients the decrease in CI exceeded 20%, suggesting a subpopulation of especially susceptible individuals. High initial CI, age, pre-existent heart disease, and severity of cirrhosis did not predict greater vulnerability. Adding an infusion of nitroprusside regularly reverted CI to control levels, regardless of the extent of cardiac output depression. Vasopressin was 38% as effective as a subsequent shunt in reducing splanchnic venous pressure. The portal hypotensive action bore no relationship to CI, but the pressure decrease caused by vasopressin was predictive of the reduction that could be achieved by shunting. The effects of the two types of shunts on systemic hemodynamics were minor and remarkably similar.

Topics: Adult; Aged; Blood Pressure; Cardiac Output; Female; Heart; Hemorrhage; Humans; Hypertension, Portal; Male; Middle Aged; Nitroprusside; Portal System; Portasystemic Shunt, Surgical; Vasopressins

Topics: Angiotensin II; Animals; Blood Volume; Evoked Potentials; Female; Hemorrhage; Neural Inhibition; Neurosecretion; Paraventricular Hypothalamic Nucleus; Rats; Rats, Inbred Strains; Vasopressins; Water-Electrolyte Balance

Plasma renin activity (PRA) was measured in conscious Brattleboro strain, vasopressin (AVP)-deficient diabetes insipidus (DI) and heterozygous rats with the aid of chronically implanted catheters. Baseline, dehydration-stimulated, and hemorrhage-stimulated levels of PRA were elevated in DI rats, as compared to levels in heterozygous controls. Replacement therapy with either AVP or the nonpressor AVP analog dDAVP reduced PRA to control levels. The high level of PRA in DI rats was associated with the lack of endogenous antidiuretic activity per se and not the pressor activity associated with the vasopressin molecule. Thus, elevated PRA in the chronic absence of AVP (in DI rats) most probably results indirectly from the chronically reduced plasma volume reported associated with hypothalamic diabetes insipidus.

Topics: Animals; Consciousness; Dehydration; Hemorrhage; Rats; Rats, Brattleboro; Rats, Mutant Strains; Renin-Angiotensin System; Vasopressins

Topics: Adrenal Cortex Hormones; Adrenocorticotropic Hormone; Animals; Blood Pressure; Body Temperature; Disease Models, Animal; Dogs; Female; Hemorrhage; Male; Rectum; Renin; Vasopressins

Spontaneous blood pressure recovery following hemorrhage in anesthetized rats is almost completely blocked by administration of captopril. This occurs despite comparable or enhanced increases in plasma levels of catecholamines and vasopressin. These findings suggest that angiotensin II, the formation of which is blocked by captopril, is essential to acute blood pressure recovery following hemorrhage and that changes in catecholamines or vasopressin are insufficient to sustain pressure recovery. The data also indicate that angiotensin II formation is not essential in the hemorrhagic stimulation of vasopressin or catecholamines.

Topics: Animals; Blood Pressure; Captopril; Cardiovascular System; Catecholamines; Hemorrhage; Male; Proline; Rats; Rats, Inbred Strains; Sympathetic Nervous System; Vasopressins

The role of vasopressin in the regulation of blood pressure during nonhypotensive hemorrhage was assessed in conscious dogs. An antagonist of the vasoconstrictor activity of vasopressin was administered (10 microgram/kg) to four normal dogs five min prior to the commencement of a 15 min arterial hemorrhage (1 ml/kg/min). The withdrawn blood was reinfused 15 min after completion of the hemorrhage. In the absence of vasopressin blockade, blood pressure and heart rate did not change significantly, while plasma renin activity increased from 3.8 +/- 0.9 to 10.8 +/- 3.1 ng/ml/3h (P less than 0.005), and plasma corticosteroid concentration increased from 1.5 +/- 0.8 to 8.6 +/- 2.0 microgram/dl (P less than 0.001). Following vasopressin blockade, the same hemorrhage decreased mean arterial pressure from 96 +/- 264 +/- 7 mmHg (P less than 0.001), increased heart rate from 71 +/- 10 to 130 +/- 23 beats/min (P less than 0.05), increased plasma renin activity from 7.1 +/- 0.8 to 30.3 +/- 6.7 ng/ml/3h (P less than 0.005) and increased plasma corticosteroid concentration from 1.9 +/- 0.7 to 11.4 +/- 1.2 microgram/dl (P less than 0.001). These data indicate that vasopressin plays an important role in blood pressure regulation during mild hemorrhage in conscious dogs.

Topics: Adrenal Cortex Hormones; Animals; Arginine Vasopressin; Blood Pressure; Dogs; Female; Heart Rate; Hemorrhage; Renin; Vasopressins

Topics: Adolescent; Adult; Angiography; Embolization, Therapeutic; Female; Gelatin Sponge, Absorbable; Hemorrhage; Hemostatic Techniques; Humans; Male; Spleen; Splenic Artery; Steel; Vasopressins

In the anesthetized dog, the concentrations of vasopressin (ADH) in plasma and cerebrospinal fluid (CSF) were similar under basal conditions, and there was a highly significant positive correlation between them (r = 0.71, p less than 0.01). Although hemorrhage was capable of increasing the ADH concentration in both plasma and CSF, the threshold for the increase in plasma ADH was much lower than for the increase in the concentration of ADH in CSF. In addition, the magnitude of the increase in the concentration of ADH in plasma was considerably greater than that in CSF at a comparable degree of hemorrhage. Our results suggest that ADH released into CSF during hemorrhage may have a different origin from that released into blood.

Topics: Animals; Dogs; Hemorrhage; Kinetics; Male; Osmolar Concentration; Potassium; Sodium; Vasopressins

Repeated withdrawal of 15 ml arterial blood at 10 min intervals produced marked hypovolaemia and hypotension with plasma vasopressin concentration increasing exponentially from 53 microE/ml to more than 700 microE/ml contrary to the hypovolaemia. After the first blood withdrawal there exists a linear correlation between the increase of the plasma vasopressin concentration and the decrease of the mean arterial blood pressure. With 61.5 microE/ml the cerebrospinal fluid withdrawn following the last bleeding likewise showed a very high vasopressin level. After extraction of the hormone from plasma and cerebrospinal fluid the vasopressin concentration was determined by means of the antidiuretic bioassay in the water-loaded rat.

Topics: Animals; Blood Pressure; Female; Hemorrhage; Male; Rabbits; Vasopressins

The effects of alterations of plasma osmolality on plasma arginine vasopressin (AVP) and renin activity (PRA) following graded hemorrhage were studied in conscious dogs who were either euhydrated, dehydrated, water loaded, or infused with hypertonic saline. Base-line plasma osmolality and AVP were significantly different in the four treatment groups; however, following hemorrhage the increases in log AVP did not significantly differ. An unexpected finding was that water loading resulted in significant elevations in PRA and plasma aldosterone concentrations, whereas plasma osmolality and AVP were reduced. Prior to hemorrhage, PRA was significantly greater in the water-loaded and dehydrated groups than in the euhydrated or saline-infused groups; following hemorrhage the increases in log PRA were not significantly different in all four treatment groups. The data suggest that, although alterations in osmolality influence base-line levels of AVP, they have no effect on relative (logarithmic) rises in AVP following hemorrhage. Similarly, alterations in AVP may influence base-line PRA, but do not influence relative rises in PRA following hemorrhage.

Topics: Animals; Blood Physiological Phenomena; Blood Pressure; Dehydration; Dogs; Hemorrhage; Kidney; Male; Osmolar Concentration; Renin; Vasopressins

It is known that vasopressin decreases PRA and heart rate and increases blood pressure and plasma corticosteroid concentration. The purpose of this study was to determine the plasma concentration of vasopressin required to produce these effects. Arginine vasopressin was administered iv to five normal conscious dogs as priming injections of 0.1, 0.5, 1.0, 2.5, 5.0, and 10.0 ng/kg, followed by infusions of 0.01, 0.05, 0.1, 0.25, 0.5, and 1.0 ng/kg x min, respectively, for 30 min. These doses produced increases in the plasma vasopressin concentration (+/- SE) of 1.0 +/- 0.8, 2.1 +/- 4.3, 4.3 +/- 1.8, 11.4 +/- 1.0, 19.7 +/- 6.4, and 30.8 +/- 7.8 pg/ml, respectively, from a basal level of 2.7 +/- 0.2 pg/ml. An increase in the plasma vasopressin concentration of 2.1 +/- 0.3 pg/ml suppressed PRA by 19 +/- 5% (P < 0.02); increases of 4.2 +/- 1.8 pg/ml or more suppressed PRA by 34 +/- 12% (P < 0.005). Only the highest dose of vasopressin produced a significant pressor effect (9 +/- 3 mm Hg; P < 0.05) or lowered the heart rate (18 +/- 4 beats/min; P < 0.005). An increase in plasma vasopressin concentration of 19.7 +/- 6.4 pg/ml was required to increase the plasma corticosteroid concentration (1.2 +/- 0.2 to 2.2 +/- 0.4 microgram/dl; P < 0.01); the largest dose of vasopressin increased the plasma corticosteroid concentration from 1.5 +/- 0.1 to 2.4 +/- 0.6 microgram/dl (P < 0.02). Twenty-four-hour water deprivation in the same dogs increased the plasma vasopressin concentration from 2.5 +/- 0.2 to 7.4 +/- 0.6 pg/ml (P < 0.01). Nonhypotensive hemorrhage in another group of dogs increased the plasma vasopressin concentration from 2.5 +/- 0.2 to 47.4 +/- 16.8 pg/ml (P < 0.05). These data indicate that elevations in the plasma vasopressin concentration within the range observed during 24 h of water deprivation and nonhypotensive hemorrhage produced significant decreases in renin secretion and heart rate and elevations in blood pressure and corticosteroid secretion.

Topics: Adrenal Cortex Hormones; Animals; Arginine Vasopressin; Blood Pressure; Dogs; Female; Heart Rate; Hemorrhage; Kinetics; Osmolar Concentration; Renin; Vasopressins; Water Deprivation

Topics: Angiography; Embolization, Therapeutic; Hemorrhage; Humans; Vasopressins

Topics: Animals; Blood Pressure; Dogs; Feedback; Hematocrit; Hemorrhage; Nephrectomy; Norepinephrine; Osmolar Concentration; Potassium; Reflex, Abnormal; Sodium; Spinal Cord; Vasopressins

A radioimmunoassay of ADH has been applied to the study of plasma ADH levels in various conditions. The validity of the assay has been evaluated by the usual quality control parameters of RIA and by the measure of plasma levels in 12 upright water deprived normal volunteers (mean 9.5 pg/ml, SEM +/- 1.5) in 8 resting and hydrated normal volunteers (1.3 +/- 0.4 pg/ml), in a case of diabetes insipidus (1.6 pg/ml), in 8 cases of SIADH Syndrome (range 13-77 pg/ml) and in 4 anesthetized dogs before (33.7 +/- 9.2 pg/ml) and after acute haemorrhage (66 +/- 9.5 pg/ml, p less than 0.02). The osmotoic challenge to ADH secretion has been studied in 8 patients with no overt endocrine pathology by salt perfusion and showed a significant rise (p less than 0.05) of plasma ADH from 6.3 +/- 3.1 pg/ml before, to 20.6 +/- 7.9 pg/ml during salt infusion corresponding to the significant (p less than 0.0001) rise of plasma osmolality from 273 +/- 2.8 to 288.2 +/- 1.1 m Osm/kg.

Topics: Animals; Dehydration; Diabetes Insipidus; Dogs; Hemorrhage; Humans; Inappropriate ADH Syndrome; Osmolar Concentration; Radioimmunoassay; Saline Solution, Hypertonic; Vasopressins

Experiments performed on male Wistar, Long Evans and Brattleboro rats indicate that the latter strain of animals, lacking vasopressin in their posterior pituitaries, are extremely sensitive to hemorrhagic and bowel ischemic shock. Mild forms of both hemorrhagic and bowel ischemic shock, as produced in Wistar or Long Evans rats, results in marked hypotension, hemoconcentration and blockade of the reticuloendothelial system (RES) in Brattleboro animals of similar sex, age and weight. These direct findings indicate that release of endogenous vasopressin in shock syndromes may be critical in maintenance of circulatory homeostasis and RES function.

Topics: Animals; Blood Pressure; Hematocrit; Hemorrhage; Intestines; Ischemia; Male; Mononuclear Phagocyte System; Phagocytosis; Rats; Shock; Species Specificity; Vasopressins

In four mature chronically catheterized fetal sheep in utero arterial pressure, heart rate, arterial pH and haematocrit fell during a 16-70% haemorrhage, while Pao2 rose. Plasma vasopressin concentrations increased and were correlated with the percentage of blood volume removed. Following haemorrhage arterial pressure and heart rate were restored within 60 min, while hyperozaemia and acidaemia persisted. Plasma antidiuretic hormone (ADH) concentrations remained the same or increased and were significantly related to the degree of acidaemia. Upon return of the removed blood, pressure rose transiently and Pao2 fell; pH remained low and plasma ADH concentrations fell, but were still related to the degree of acidaemia. In three immature, exteriorized fetuses (0.4 of term) plasma vasopressin concentrations also rose during haemorrhage. The results indicate that fetal plasma vasopressin levels rise during haemorrhage in response both to hypovolaemia and the subsequent acidaemia. Further the response to haemorrhage is present at an early gestational age.

Topics: Animals; Blood Pressure; Female; Fetal Blood; Fetus; Heart Rate; Hemorrhage; Hydrogen-Ion Concentration; Pregnancy; Sheep; Time Factors; Vasopressins

Excessive bleeding from the head and neck sometimes presents a therapeutic problem. Ten patients with this type of haemorrhage have been treated with continous vasopressin infusion for 1-3 days. Haemostasis was quickly established in eight cases. No serious side effects were noted. Infusion of vasopressin has a rapid, beneficial effect on haemorrhage from branches of the external carotid artery.

Topics: Adolescent; Adult; Aged; Carotid Artery, External; Child; Epistaxis; Female; Hemorrhage; Hemostasis; Humans; Male; Middle Aged; Oral Hemorrhage; Time Factors; Vasopressins

Topics: Acute Disease; Animals; Blood Pressure; Blood Volume; Cardiac Output; Dogs; Hemorrhage; Liver Circulation; Portal System; Vasopressins

1. The possible pressor effect of vasopressin immediately after acute haemorrhage has been studied using anaesthetized Brattleboro rats with diabetes insipidus and rats of the Long Evans parent strain.2. A blood loss of 0.5% of the body weight caused a significant decrease in mean arterial blood pressure, measured 10 min later, in Brattleboro rats, whereas this degree of haemorrhage was non-hypotensive in the control Long Evans rats. Following subsequent blood losses (each of 0.5% of the body weight), mean arterial blood pressure in Brattleboro rats was always significantly lower than in Long Evans rats.3. While no antidiuretic activity was at any time found in the plasma of Brattleboro rats, haemorrhages greater than 1% of the body weight were associated with marked increases in plasma arginine vasopressin (AVP) of Long Evans rats.4. When Brattleboro and Long Evans rats were subjected to a single haemorrhage of 2% of the body weight, the immediate decrease in arterial blood pressure was similar in the two groups. However, 5 and 10 min after the haemorrhage the arterial blood pressure was significantly higher in the Long Evans rats. When vasopressin was infused into Brattleboro rats so that plasma levels of the hormone approached those found in Long Evans rats, the mean arterial blood pressure 0, 5 and 10 min after haemorrhage was similar to that in the Long Evans animals.5. It is concluded that in the anaesthetized rat, vasopressin plays an important role in the regulation of arterial blood pressure during the period immediately following acute haemorrhage.

Topics: Animals; Blood Pressure; Diabetes Insipidus; Heart Rate; Hemorrhage; Male; Rats; Vasopressins

1. The role of vasopressin in blood pressure control and in the pathogenesis of one-kidney Goldblatt hypertension in the conscious dog was investigated. 2. Infusion of synthetic arginine vasopressin to elevate plasma levels approximately five-fold caused bradycardia in normal dogs and increase in mean arterial blood pressure in dogs with pharmacological autonomic blockade. 3. A similar degree of elevation of plasma vasopressin concentration was observed after mild non-hypotensive haemorrhage. 4. Renal artery constriction in unilaterally-nephrectomized dogs caused a rise in plasma renin activity and only a doubling of plasma vasopressin concentration, but a marked rise in mean arterial blood pressure. 5. Vasopressin may play a role in normal cardiovascular homeostatic responses, but its role in the pathogenesis of this form of hypertension is unlikely to be significant.

Topics: Animals; Autonomic Nervous System; Blood Pressure; Dehydration; Dogs; Hemorrhage; Hypertension, Renal; Hypertension, Renovascular; Male; Vasopressins

Topics: Adult; Female; Foot Diseases; Gangrene; Hemorrhage; Humans; Infusions, Parenteral; Mesenteric Arteries; Radiography; Renal Artery; Stevens-Johnson Syndrome; Vasopressins

Topics: Animals; Blood Pressure; Dogs; Female; Hemorrhage; Male; Models, Biological; Plasma Volume; Regression Analysis; Vasopressins

Massive bleeding owing to cyclophosphamide-induced hemorrhagic cystitis was not affected by intravesical instillation of 4 per cent formalin or 1 per cent silver nitrate. After initiation of a continuous systemic infusion of vasopressin hematuria and transfusion requirements diminished markedly. Adverse reactions were mild. Intravenous vasopressin was a safe and effective means to control temporarily life-threatening hemorrhagic cystitis.

Topics: Adolescent; Cyclophosphamide; Cystitis; Hemorrhage; Humans; Male; Urinary Bladder Diseases; Vasopressins

Topics: Action Potentials; Animals; Female; Hemorrhage; Hypothalamus; Hypothalamus, Anterior; Lactation; Oxytocin; Pregnancy; Rats; Vasopressins

1-Deamino-8-d-arginine vasopressin (D.D.A.V.P.) infusion causes a marked increase in factor-VIII (antihaemophilic-factor)-related properties in patients with moderate and mild haemophilia and von Willebrand's disease (vWd). The possibility was therefore evaluated that such an autologous factor-VII response might be haemostatically effective, allowing patients to undergo surgery without plasma concentrates. 0.3 microng/kg of D.D.A.V.P. given before dental surgery and repeated in the early postoperative period was followed by a two to three fold rise in factor-VIII coagulant activity (VII C.A.) in four patients with moderate and mild haemophilia. In two, there was no abnormal bleeding after dental extraction, whereas plasma concentrates were necessary to control oozing from the sockets in the remaining two patients. A higher D.D.A.V.P. dosage (0.4-0.5 microng/kg) in patients with higherstarting VII C.A. (9% or more) was followed by a more marked response (four to six fold). VII C.A. levels up to 100% of average normal were achieved and dental extraction and major surgery (such as cholecystectomy, thoracotomy, and two tonsillectomies) were carried out successfullly in six patients with mild haemophilis and in two with vWd. The mean half-life of autologous VII C.A. was 9.4 h (range 7.5-11.6). Plasma and urine osmolality showed no consistent variation after drug administration. Thus D.D.A.V.P. appears a promision pharmacological alternative to plasma concentrates in the management of some patients with haemophilis and vWd.

Topics: Adolescent; Adult; Biopsy; Blood Coagulation Tests; Cholecystectomy; Deamino Arginine Vasopressin; Drug Evaluation; Factor VIII; Female; Hemophilia A; Hemorrhage; Hemostasis, Surgical; Humans; Infusions, Parenteral; Male; Middle Aged; Postoperative Care; Postoperative Complications; Preoperative Care; Thoracic Surgery; Thorax; Tonsillectomy; Tooth Extraction; Vasopressins; von Willebrand Diseases

Topics: Blood Coagulation; Deamino Arginine Vasopressin; Hemophilia A; Hemorrhage; Humans; Vasopressins; von Willebrand Diseases

Topics: Arginine Vasopressin; Drug Evaluation; Female; Hemophilia A; Hemorrhage; Hemostasis, Surgical; Hemostatics; Humans; Postoperative Care; Postoperative Complications; Preoperative Care; Vasopressins; von Willebrand Diseases

Topics: Angiography; Embolization, Therapeutic; Gastrointestinal Hemorrhage; Gelatin; Hemorrhage; Humans; Male; Middle Aged; Vasopressins

Selective arterial infusions of vasopressin have often been successful in controlling arterial bleeding. When bleeding occurs in an area with a dual blood supply through a vascular arcade, situations may arise which can compromise angiographic management. These include: (1) artifacts caused by pressure injections of contrast material inaccurately depicting the usual distribution of blood flow in the arcade; (2) catheter-induced vasospasm altering the flow dynamics through the arcade; (3) vasopressin-induced constriction of the proximal portion of an arcade changing the origin of blood flow to the distal arcade; and (4) proximal occlusion of one limb of an arcade permitting continuation of bleeding through collateral channels. When angiographic techniques fail to control bleeding because of these circumstances, hemostasis may be achieved by treating both limbs of the vascular arcade.

Topics: Angiography; Catheterization; Collateral Circulation; Hemorrhage; Humans; Regional Blood Flow; Vasoconstrictor Agents; Vasopressins

Using unanaesthetized monkeys, experiments were performed to examine the effects of haemorrhage on the liberation of arginine vasopressin (AVP). Haemorrhages of 10%, 15% or 20% total blood volume were performed via a catheter with its tip in the abdominal vena cava. A catheter in the left internal jugular vein was used for blood sampling. Arterial blood pressure was monitored via a catheter whose tip resected in an iliac artery. The monkeys showed no signs of discomfort from this catheterisation. Blood samples for AVP assay were taken at different times from 0-90 min after the end of the haemorrhage. At the end of the experiment, blood removed was reinfused. Results show that haemorrhage resulted in liberation of AVP, but only if there was a fall in arterial blood pressure. AVP release occurred more readily as the total volume of blood withdrawn increased, but the absolute rise in hormone concentration was not related to the total volume of blood withdrawn. However, comparing the area under the curve of mean arterial blood pressure with that for AVP concentration showed the two to have a significant exponential relationship. It is concluded that, as in other species, haemorrhage is a potent stimulus for AVP liberation in the monkey. However, in contrast to some other species, the fall in arterial pressure seems to be the prime stimulus rather than hypovolemia per se.

Topics: Animals; Arginine Vasopressin; Blood Volume; Haplorhini; Heart Rate; Hemorrhage; Hypotension; Macaca mulatta; Male; Respiration; Vasopressins

Acute hemorrhagic pancreatitis was created in dogs using the closed duodenal loop technique. After 18 hours, a a constant rate of pancreatic exocrine secretion was stimulated with secretin. A direct relationship was observed between the percentage inhibition of secretin-stimulated pancreatic exocrine flow and the dose of antidiuretic hormone administered to dogs with acute hemorrhagic pancreatitis. The acute hemorrhagic pancreatitis reduced the sensitivity of the exocrine pancreas to secretin and antidiuretic hormone.

Topics: Acute Disease; Animals; Disease Models, Animal; Dogs; Hemorrhage; Pancreas; Pancreatitis; Secretin; Vasopressins

Two days after a severe haemorrhage plasma calcium concentrations and bone marrow mitotic activity in rats were significantly increased and so remained for a further 5-6 days until the haematocrit had returned to normal. The first 48 h after bleeding were characterized by hypocalcaemia. During this phase two significant peaks in mitotic activity were observed at 4 and 18 h after haemorrhage. The mitotic surge 4 h after bleeding was still present in adrenalectomized and parathyroidectomized animals but in rats which were either hypophysectomized or had congenital diabetes insipidus this mitotic response was absent. Vasopressin was shown to stimulate bone marrow mitotic activity both in vivo and in vitro whereas angiotensin, aldosterone and erythropoietin had no rapid, direct mitogenic action on these cells. This novel hypophysial-bone marrow system suggests that vasopressin may assist in post-haemorrhagic recovery in blood cell numbers in the circulation.

Topics: Animals; Bone Marrow; Bone Marrow Cells; Calcium; Hematocrit; Hemorrhage; Hypophysectomy; Male; Mitosis; Rats; Time Factors; Vasopressins

Vasopressin (antidiuretic hormone, ADH), release in response to hemorrhage was studied in spontaneously hypertensive rats (SHR), Kyoto-Wistar rats (KWR), and Wistar rats (WR). The rats were anesthetized with pentobarbital sodium and ADH concentration was measured before and after three successive hemorrhages at 15 min intervals. The blood samples for radioimmunoassay (RIA) of ADH were collected from the external jugular vein. The ADH release in response to hemorrhage was significantly reduced in debuffered WR (carotid and aortic baroceptors and atrioventricular receptors deafferented), intact KWR and intact SHR when compared to the intact WR.

Topics: Animals; Chemoreceptor Cells; Hemorrhage; Hypertension; Male; Pressoreceptors; Rats; Vasopressins

The effectiveness of ornipressin and adrenaline as local vasoconstrictors is compared, with special reference to cleft-lip-and-palate surgery. A latent period of 3 - 5 minutes with the use of ornipressin is advised. A brief review comparing the local and general effects of ornipressin and adrenaline is included.

Topics: Cleft Lip; Cleft Palate; Epinephrine; Hemorrhage; Hemostasis, Surgical; Humans; Infant; Infant, Newborn; Ornithine; Vasopressins

A radioimmunoassay has been developed for plasma arginine-vasopressin in man and dog. The mean recovery of added arginine-vasopressin (AVP) was 60 +/-6.9 (S.D.)% and the lower threshold of detection 2.0 pmol/1. A close correlation was found between concurrent radioimmunoassay and bioassay values. The mean concentration found in peripheral venous blood in healthy men after overnight fasting was 5.3 pmol/1 (range 4.6-6.2 pmol/1.) In man, significant increases in plasma AVP occurred after dehydration (5-9-9-5 pmol/1) and significant decreases after oral water-loading (5.9-9.5 pmol/1). During i.v. infusion of graded doses of synthetic AVP in normal men, plasma levels were closely correlated with infusion rate. On stopping the infusion, plasma vasopressin fell exponentially with a half-life of between 7 and 8 min. In man, plasma AVP was unaffected by tilting head-up for 2 h, or by a non-hypotensive bleeding of 500 ml in 10 min. In the dog, haemorrhage of 5 ml/kg and over caused proportionate increases in AVP in the circulation. In normal men, plasma vasopressin was significantly correlated with concurrent urinary osmolality. Five patients with oat-cell bronchial carcinoma and hyponatraemia showed a marked increase of plasma vasopressin. Five patients with diabetes insipidus had significantly reduced, but detectable, levels of plasma AVP. The plasma concentration in these patients did not increase after water restriction.

Topics: Adult; Animals; Arginine Vasopressin; Biological Assay; Blood Volume; Bronchial Neoplasms; Carcinoma, Small Cell; Dehydration; Diabetes Insipidus; Dogs; Half-Life; Hemorrhage; Humans; Male; Osmolar Concentration; Posture; Radioimmunoassay; Urine; Vasopressins; Water; Water Deprivation

Topics: Accidents, Traffic; Adult; Anti-Bacterial Agents; Brain Concussion; Catheterization; Central Venous Pressure; Chlorides; Diabetes Insipidus; Female; Hemorrhage; Humans; Hydrogen-Ion Concentration; Infusions, Parenteral; Intracranial Pressure; Maxillofacial Injuries; Skull; Sodium; Urinary Catheterization; Vasopressins; Water; Water Intoxication

Topics: Animals; Dopamine; Electric Stimulation; Half-Life; Hemorrhage; Neurophysins; Oxytocin; Perfusion; Pituitary Gland, Posterior; Radioimmunoassay; Rats; Swine; Vasopressins

The hypothesis that receptors in the heart or pulmonary vasculature initiate a reflex that influences urine flow was derived from experiments designed to evaluate the effect of mechanical ventilation on renal function. These experiments indicated that urine flow usually decreases during positive-pressure breathing and usually increases during negative-pressure breathing. It was surmised that impulses from certain cardiopulmonary receptors affect the secretion of ADH, which in turn influences urine flow. A subsequent investigation appeared to localize the pertinent receptors to the left atrium, but the results of this particular investigation were influenced by several complication factors that have not been widely appreciated. The apparent localization of volume-regulating recpetors to the left atrium and the accumulating evidence that atrial receptors do respond to changes in atrial pressure or atrial volume triggered a myriad of further studies on the function of left receptors. Nearly all these studies employed indirect techniques that produced changes in systemic and pulmonary hemodynamics in addition to changes in left atrial pressure. Nevertheless, it often was assumed that if changes in left pressure were produced, any concomitant changes in circulating ADH or in urine flow were attributable to a reflex elicited from atrial receptors. Mush of the data obtained were interpreted as being compatible with the elft atrial volume-receptor hypothesis, but very liggle of the data pertained to left atrial receptors specifically.

Topics: Animals; Atrial Function; Biological Assay; Blood Pressure; Blood Volume; Cardiac Surgical Procedures; Cardiac Tamponade; Denervation; Diuresis; Dogs; Extracellular Space; Heart Failure; Hemorrhage; Hypothalamus; Immersion; Kidney; Mechanoreceptors; Natriuresis; Nerve Fibers, Myelinated; Positive-Pressure Respiration; Posture; Radioimmunoassay; Regional Blood Flow; Sensory Receptor Cells; Tachycardia; Vagotomy; Vagus Nerve; Vasopressins; Veratridine

Antidiuretic hormone had a marked effect on the microscopic anatomy of the pancreas and the duodenum subjected to a closed duodenal loop obstruction. In contrast to the acute hemorrhagic pancreatitis usually seen, the pancreas showed only a slight extravasation of red and white blood cells into the connective tissue spaces, some blood vessel engorgement and a slight edema. No tissue disruption of the pancreas was observed. The appearance of the closed loops were also modified by the antidiuretic hormone. These closed loops contained small amounts of fluid with little odor and the duodenal villi showed little or no necrosis. Antidiuretic hormone also reduced the amylase concentration and the fluid volume in the peritoneal cavity and in the closed duodenal loop.

Topics: Animals; Body Fluids; Dogs; Duodenum; Hemorrhage; Pancreas; Pancreatitis; Vasopressins

Topics: Abdomen; Adult; Blood Pressure; Cardiac Output; Esophageal and Gastric Varices; Female; Headache; Heart Rate; Hemorrhage; Humans; Infusions, Parenteral; Injections, Intravenous; Male; Middle Aged; Muscle Cramp; Nausea; Vasopressins

These experiments were designed to determine whether angiotensin II (AII) could potentiate the increase in plasma vasopressin (ADH) concentration produced by continuous, nonhypotensive hemorrhage in nephrectomized dogs. Infusion of AII (10 ng/kg.min) into a common carotid artery in nonbled dogs did not increase plasma ADH levels, suggesting that increases in carotid arterial plasma AII concentration alone do not stimulate an increase in ADH release. Subsequently, nephrectomized dogs subjected to nonhypotensive hemorrhage (0.44 ml/kg.min) were infused as follows: 0.9% saline intravenously, AII (10 ng/kg.min) intravenously, or AII (10 ng/kg.min) into the carotid. The Plasma ADH concentration increased in all three groups of dogs during hemorrhage. Although the AII-infused dogs demonstrated significant increases in plasma ADH levels earlier during hemorrhage, these changes were small; there were no statistically significant differences in plasma ADH concentrations among the three groups. These results suggest that increases in plasma AII concentration have little or no significant effect on the volume control of ADH release.

Topics: Angiotensin II; Animals; Blood Pressure; Carotid Arteries; Central Venous Pressure; Dogs; Heart Rate; Hematocrit; Hemorrhage; Injections, Intra-Arterial; Injections, Intravenous; Kidney; Male; Nephrectomy; Osmolar Concentration; Potassium; Renin; Sodium; Stimulation, Chemical; Vasopressins

Topics: Animals; Arginine Vasopressin; Bone Marrow; Bone Marrow Cells; Hemorrhage; In Vitro Techniques; Mitosis; Rats; Vasopressins

Topics: Action Potentials; Animals; Blood Pressure; Female; Hemorrhage; Hypothalamus; Lactation; Paraventricular Hypothalamic Nucleus; Pregnancy; Rats; Time Factors; Vasopressins

Acute volume expansion was produced in 9 dogs by infusing a lactated Ringer's solution at 1 ml/kg/min in a volume estimated to increase blood volume by 20%. Volume expansion was maintained by replacing urinary fluid losses with equal volumes of the Ringer's solution. Following volume expansion, the effects of a slow, nonhypotensive hemorrhage on plasma antidiuretic hormone concentration (PADH) were determined and compared to a group of 9 normovolemic dogs subjected to the same hemorrhage procedure, in order to determine if volume receptor control of ADH release would adapt to acute increases in blood volume. Ringer's infusion significantly increased blood volume to 95.2 +/- 3.1 ml/kg (mean +/- SE; P less than 0.01) when compared to a mean normovolemic blood volume of 77.6 +/- 3.4 ml/kg. Volume expansion was associated with a significantly lower PADH (3.2 +/- 1.6 muU/ml) than that in normovolemic dogs (5.7 +/- 1.2 muU/ml; p less than 0.05). Significant increases in PADH (P less than 0.05) occurred in both groups of dogs after 20 and 40 minutes of a continuous, nonhypotensive hemorrhage (0.40 to 0.45 mg/kg/min. Hemmorrhage was also associated with significant decrease in effective left atrial pressure in both groups of dogs after 5, 10, 20, and 40 minutes of hemorrhage (P less than 0.01). There were no significant differences between the two groups of dogs nor were there any significant changes during the experiment within each group for mean arterial blood pressure, arterial pulse pressure, plasma osmolality, plasma sodium concentration and plasma potassium concentration. Effective left atrial pressure and PADH were found to be exponentially correlated with blood volume in bothy hypervolemic and normovolemic dogs. Analysis of covariance of these correlations suggested that the hypervolemic dogs exhibited the same exponential changes in PADH and effective left atrial pressure with decreased blood volume as in the normovolemic dogs. It is concluded that acute volume expansion does not alter volume control of plasma ADH concentration.

Topics: Anesthesia, General; Animals; Blood Pressure; Blood Volume; Dogs; Hemorrhage; Male; Osmolar Concentration; Potassium; Pulse; Sodium; Vasopressins

Topics: Adult; Aged; Embolization, Therapeutic; Female; Genital Neoplasms, Female; Hemorrhage; Humans; Injections, Intra-Arterial; Middle Aged; Vasopressins

Topics: Animals; Blood; Carotid Arteries; Cattle; Female; Hemorrhage; Neurophysins; Osmolar Concentration; Pituitary Gland, Posterior; Vasopressins

Topics: Absorption; Aldosterone; Angiotensin II; Animals; Biological Assay; Biological Transport, Active; Blood Volume; Dogs; Extracellular Space; Female; Hemorrhage; Ileum; Male; Rats; Sodium; Vasopressins

Topics: Angiotensin II; Animals; Bradykinin; Epinephrine; Hemorrhage; Hexamethonium Compounds; Histamine; Hypertension, Pulmonary; Intracranial Pressure; Male; Norepinephrine; Organ Size; Pentolinium Tartrate; Phenoxybenzamine; Pulmonary Edema; Rats; Serotonin; Stereotaxic Techniques; Vagotomy; Vagus Nerve; Vasoconstrictor Agents; Vasopressins

Topics: Adrenocorticotropic Hormone; Animals; Biological Assay; Blood Pressure; Cross Reactions; Female; Fetus; Gestational Age; Growth Hormone; Guinea Pigs; Heart Rate; Hemorrhage; Iodine Radioisotopes; Oxytocin; Pituitary Gland; Pregnancy; Pregnancy Complications, Hematologic; Radioimmunoassay; Rats; Sheep; Spectrometry, Fluorescence; Time Factors; Vasopressins

Topics: Adrenal Glands; Adrenocorticotropic Hormone; Animals; Chlorpromazine; Corticotropin-Releasing Hormone; Diabetes Insipidus; Disease Models, Animal; Ethyl Ethers; Hemorrhage; Hypothalamo-Hypophyseal System; Laparotomy; Male; Morphine; Pentobarbital; Pituitary Gland; Pituitary-Adrenal System; Rats; Stress, Physiological; Vasopressins

Topics: Angiotensin II; Animals; Bradykinin; Central Venous Pressure; Dexamethasone; Dogs; Dose-Response Relationship, Drug; Epinephrine; Glucocorticoids; Hemorrhage; Injections, Intra-Arterial; Methylprednisolone; Norepinephrine; Ouabain; Pancreas; Perfusion; Prostaglandins; Regional Blood Flow; Vasopressins

Topics: Animals; Blood Pressure; Female; Hemorrhage; Hypotension; Male; Phenoxybenzamine; Phentolamine; Pituitary Gland, Posterior; Rats; Vasopressins

Topics: Adult; Blood Pressure; Blood Volume; Female; Heart Rate; Hemorrhage; Humans; Male; Middle Aged; Osmolar Concentration; Potassium; Renin; Sodium; Vasopressins

Topics: Administration, Topical; Adolescent; Adult; Animals; Blood Pressure; Dogs; Dose-Response Relationship, Drug; Drug Evaluation; Esophageal Diseases; Esophagoscopy; Female; Glomerular Filtration Rate; Hemorrhage; Humans; Kidney; Male; Mesenteric Arteries; Middle Aged; Perfusion; Regional Blood Flow; Urination; Vasopressins

Topics: Alcoholism; Esophageal and Gastric Varices; Hemorrhage; Humans; Hypothermia, Induced; Ligation; Liver Cirrhosis; Pituitary Hormones, Posterior; Portacaval Shunt, Surgical; Pressure; Stomach; Vasopressins

Topics: Animals; Atrial Function; Blood Pressure; Blood Volume; Bloodletting; Dogs; Hemorrhage; Male; Pulse; Renin; Time Factors; Vasopressins

Topics: Adolescent; Adult; Aged; Bronchoscopy; Child; Drug Combinations; Female; Hemorrhage; Hemostasis; Humans; Male; Middle Aged; Ornithine; Vasoconstrictor Agents; Vasopressins

Topics: Animals; Blood Volume; Dogs; Hemorrhage; Time Factors; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Arginine; Biological Assay; Calcium Chloride; Cross Reactions; Half-Life; Hemorrhage; Hypophysectomy; Iodine Isotopes; Male; Neurophysins; Oxytocin; Radioimmunoassay; Rats; Vasopressins

Topics: Animals; Blood Pressure; Blood Transfusion; Blood Volume; Heart Rate; Hemorrhage; Hypophysectomy; Neurons; Neurons, Afferent; Pharyngeal Diseases; Rats; Sympathectomy; Time Factors; Vagus Nerve; Vasopressins

Topics: Abnormalities, Drug-Induced; Amniocentesis; Animals; Female; Fetus; Forelimb; Gestational Age; Hemorrhage; Hindlimb; Pregnancy; Rats; Vasopressins

1. The rabbit rectum superfused with blood or Krebs solution was used to assay vasopressin in circulating blood and in plasma extracts respectively.2. Vasopressin was released by a rapid fall in diastolic pressure of as little as 5 mmHg, and the amount of vasopressin released was proportional to the magnitude of the fall in diastolic pressure in the range studied. These results would indicate that vasopressin release follows the magnitude of the fall in diastolic pressure more closely than the actual decrease in blood volume in haemorrhagic hypotension.3. It was shown that the time required to induce an increase in circulating vasopressin is inversely proportional to the severity of the fall in diastolic pressure; this suggested that the stimulation of neurosecretory reflex arc varies with the intensity of the stimulus.4. The slight changes in plasma renin activity as well as the pattern of renin release suggested the unlikeliness of the influence of renin upon vasopressin secretion under these circumstances. On the contrary, the results suggested that the secretion of large amounts of vasopressin tended to inhibit renin release.

Topics: Animals; Ascorbic Acid; Blood Circulation; Chickens; Colon; Dose-Response Relationship, Drug; Hemorrhage; In Vitro Techniques; Muscles; Oxytocin; Rabbits; Rats; Rectum; Renin; Time Factors; Vasopressins

Topics: Animals; Female; Hemorrhage; Hyperemia; Kidney; Male; Rats; Vasopressins

Topics: Animals; Blood Gas Analysis; Blood Pressure; Cardiac Output; Coronary Circulation; Dogs; Drug Combinations; Esophageal and Gastric Varices; Heart Rate; Hemodynamics; Hemorrhage; Hepatic Artery; Hypertension; Injections, Intravenous; Isoproterenol; Liver Circulation; Portal Vein; Time Factors; Vasopressins

Topics: Aminopyrine; Animals; Bethanechol Compounds; Blood Pressure; Diffusion; Dogs; Gastric Mucosa; Hemorrhage; Histamine; Hydrochloric Acid; Injections, Intravenous; Ischemia; Norepinephrine; Pentagastrin; Sodium Chloride; Stomach Ulcer; Time Factors; Vasopressins

Topics: Animals; Blood Pressure; Blood Volume; Carotid Sinus; Denervation; Depression, Chemical; Ethanol; Glucose; Heart Rate; Hemorrhage; Hypophysectomy; Isotonic Solutions; Neurons, Afferent; Pituitary Gland; Rats; Stimulation, Chemical; Time Factors; Vagus Nerve; Vasopressins; Vena Cava, Inferior

Topics: Acute Disease; Animals; Dogs; Hemorrhage; Pancreas; Pancreatitis; Prognosis; Vasopressins

Topics: Aged; Drug Combinations; Female; Hemorrhage; Hemostasis; Humans; Male; Middle Aged; Ornithine; Postoperative Complications; Prostatectomy; Prostatic Hyperplasia; Tyrosine; Urinary Bladder; Urinary Bladder Neoplasms; Urologic Diseases; Vasopressins

Topics: Angiotensin II; Animals; Blood Pressure; Blood Volume; Dogs; Heart Rate; Hemorrhage; Kidney; Ligation; Male; Osmolar Concentration; Potassium; Regional Blood Flow; Renal Artery; Renal Veins; Renin; Respiration; Sodium; Vasopressins

Topics: Angiotensin II; Animals; Blood Pressure; Blood Volume; Dogs; Hemorrhage; Hypotension; Lymph; Metaraminol; Microcirculation; Norepinephrine; Ornithine; Oxygen; Partial Pressure; Phenylephrine; Vasoconstrictor Agents; Vasopressins

Topics: Anesthesia, Local; Epinephrine; Hemorrhage; Humans; Lidocaine; Prilocaine; Scalp; Vasoconstrictor Agents; Vasopressins

Topics: Anesthesia, General; Burns; Child; Epinephrine; Hemorrhage; Humans; Infant; Norepinephrine; Ornithine; Skin Transplantation; Transplantation, Autologous; Transplantation, Heterologous; Transplantation, Homologous; Vasoconstrictor Agents; Vasopressins

Topics: Adult; Aged; Female; Hemorrhage; Humans; Hysterectomy; Middle Aged; Postoperative Complications; Regional Blood Flow; Time Factors; Uterine Prolapse; Uterus; Vasopressins

Topics: Animals; Blood Pressure; Blood Volume; Central Venous Pressure; Dogs; Heart Rate; Hemorrhage; Hypothalamo-Hypophyseal System; Male; Methods; Osmosis; Pulse; Vasopressins

Topics: Acid-Base Equilibrium; Blood Cell Count; Cortisone; Depression; Diabetes Insipidus; Diuresis; Electrocardiography; Heart Failure; Hemorrhage; Humans; Hypophysectomy; Kidney Diseases; Methods; Pituitary Diseases; Pituitary Neoplasms; Postoperative Care; Postoperative Complications; Posture; Preoperative Care; Sodium; Time Factors; Vasopressins

Topics: Animals; Blood Pressure; Carotid Arteries; Carotid Sinus; Dogs; Hemorrhage; Pressoreceptors; Vagotomy; Vasopressins

Topics: Abdomen; Animals; Arteries; Blood Flow Velocity; Blood Pressure; Blood Volume; Dogs; Electric Stimulation; Hemorrhage; Isoproterenol; Norepinephrine; Regional Blood Flow; Splanchnic Nerves; Vascular Resistance; Vasopressins; Veins

Topics: Animals; Biological Assay; Blood Volume; Dogs; Hemorrhage; Pituitary Hormones, Posterior; Radioimmunoassay; Vasopressins

Topics: Animals; Carotid Arteries; Castration; Dairying; Female; Goats; Hemorrhage; Lactation; Male; Oxytocin; Pituitary Hormones, Posterior; Pregnancy; Vasopressins

Topics: Adrenocorticotropic Hormone; Animals; Female; Fetal Diseases; Gestational Age; Hemorrhage; Pituitary Gland; Pregnancy; Sheep; Vasopressins

Topics: Abdomen; Adrenal Glands; Angiotensin II; Animals; Blood Pressure; Blood Vessels; Cats; Denervation; Hemorrhage; Infusions, Parenteral; Kidney; Mesenteric Arteries; Mesenteric Veins; Phenoxybenzamine; Pituitary Gland; Regional Blood Flow; Spleen; Vascular Resistance; Vasomotor System; Vasopressins

Topics: Animals; Blood Circulation; Blood Pressure; Blood Volume; Carbon Dioxide; Cardiac Output; Cardiac Volume; Cerium Isotopes; Dogs; Dye Dilution Technique; Female; Heart Rate; Hematocrit; Hemodynamics; Hemorrhage; Injections, Intravenous; Male; Oxygen; Regional Blood Flow; Strontium Isotopes; Vasopressins; Xenon

Topics: Adult; Analgesia; Anesthesia, General; Anesthetics, Local; Blood Pressure; Brain Diseases; Brain Neoplasms; Craniotomy; Epinephrine; Female; Hemorrhage; Hemostasis; Humans; Male; Middle Aged; Ornithine; Pallor; Parkinson Disease; Postoperative Complications; Pulse; Stereotaxic Techniques; Trephining; Vasoconstrictor Agents; Vasopressins; Wound Healing

Topics: Animals; Arteries; Blood Pressure; Cyanides; Dogs; Femoral Artery; Hemorrhage; Splenectomy; Vasopressins

Topics: Adolescent; Adult; Child; Child, Preschool; Esophageal and Gastric Varices; Esophagoscopy; Female; Hemorrhage; Humans; Liver Cirrhosis; Liver Function Tests; Male; Methods; Middle Aged; Portal Vein; Portography; Pressure; Vasopressins

Topics: Animals; Dogs; Female; Ferricyanides; Hemorrhage; Hypotension; Male; Vasopressins

Topics: Animals; Blood Pressure; Dogs; Ferricyanides; Hemorrhage; Sodium Chloride; Vasopressins

Topics: Animals; Arginine; Biological Assay; Hemorrhage; Male; Osmolar Concentration; Pituitary Hormones, Posterior; Radioimmunoassay; Rats; Sodium Chloride; Vasopressins; Water; Water Deprivation; Water Intoxication; Water-Electrolyte Balance

Topics: Animals; Blood Pressure; Brain; Decerebrate State; Diencephalon; Dogs; Female; Hemorrhage; Male; Osmotic Pressure; Spinal Cord; Vasopressins

1. Water-loaded rats under ethanol anaesthesia were used to determine whether bradykinin releases ADH and whether the release is a reflex response to hypotension or the result of direct stimulation of the central nervous system by the peptide.2. Intravenous injections of bradykinin caused hypotension followed by prolonged antidiuresis; both responses were dose dependent.3. The antidiuresis caused by bradykinin could not be accounted for by hypotension alone. Haemorrhage and intravenous injections of isoprenaline, which caused falls in arterial blood pressure similar to those caused by bradykinin, produced only short-lasting antidiuretic responses.4. Intracarotid injections of bradykinin caused antidiuresis with little or no preceding hypotension. No antidiuresis was produced by intracarotid injections of isoprenaline.5. After intravenous injection of bradykinin, small amounts of ADH were identified in whole blood and, on a few occasions only, in concentrated urine. However, ADH was not detected in blood extracts.6. After intravenous injection of nicotine in doses which caused antidiureses similar to that caused by bradykinin, ADH was regularly detected in large amounts in blood extracts and in unconcentrated urine.7. Bradykinin did not cause prolonged antidiureses when injected into a rat with congenital diabetes insipidus.8. ADH release was not increased when isolated rat neural lobes were incubated with bradykinin although release was elevated by an increase in the K(+) concentration of the incubation medium.9. It is suggested that bradykinin causes release of an antidiuretic substance by a direct action on the central nervous system. The possibility that this substance is ADH is discussed.

Topics: Animals; Blood Pressure; Bradykinin; Carotid Arteries; Central Nervous System; Diabetes Insipidus; Diuresis; Female; Hemorrhage; Hypotension; Injections, Intra-Arterial; Injections, Intravenous; Isoproterenol; Male; Nicotine; Pituitary Gland, Posterior; Potassium; Rats; Vasopressins

Topics: Animals; Blood Pressure; Cardiac Output; Disease Models, Animal; Dogs; Heart Atria; Heart Rate; Hemorrhage; Hypothalamo-Hypophyseal System; Mitral Valve Stenosis; Pressoreceptors; Vasopressins

Topics: Animals; Biological Assay; Bronchial Neoplasms; Carcinoma, Bronchogenic; Chlorpropamide; Diabetes Insipidus; Female; Hemorrhage; Humans; Immune Sera; Labor, Obstetric; Nicotine; Pregnancy; Radioimmunoassay; Sheep; Vasopressins

Topics: Animals; Calcium Chloride; Hemorrhage; Oxytocin; Pituitary Hormones, Posterior; Radioimmunoassay; Rats; Vasopressins

Topics: Animals; Blood Volume; Dogs; Female; Hemorrhage; Hypertonic Solutions; Jugular Veins; Kidney Concentrating Ability; Male; Osmolar Concentration; Sodium Chloride; Vasopressins

1. Splenic arterial flow and splenic weight were recorded in cats anaesthetized with sodium pentobarbitone. The responses of the spleen to catecholamines, angiotensin and vasopressin were investigated.2. Catecholamines caused responses mediated by alpha- and beta-adrenoceptors in the arteriolar smooth muscle, but only insignificant beta-adrenoceptor responses could be elicited from the capsular smooth muscle. The difficulties in elucidating the mechanism of action of catecholamines on arteriolar smooth muscle are discussed.3. Angiotensin caused marked vasoconstriction, but contraction of the capsular smooth muscle was less marked. Vasopressin caused vasoconstriction but had no effect on capsular smooth muscle. Thus these peptides constrict the resistance vessels but produce much weaker contraction of the capsule.4. These responses are discussed in relation to the splenic responses to acute haemorrhage.

Topics: Acute Disease; Anesthesia, Intravenous; Angiotensin II; Animals; Catecholamines; Cats; Constriction; Hemorrhage; Injections, Intravenous; Muscle, Smooth; Organ Size; Pentobarbital; Regional Blood Flow; Spleen; Vasopressins

Topics: Adrenal Glands; Angiotensin II; Animals; Blood Flow Velocity; Blood Pressure; Cats; Denervation; Hemorrhage; Intestines; Kidney; Mesenteric Arteries; Phenoxybenzamine; Pituitary Gland; Regional Blood Flow; Sympathetic Nervous System; Vasomotor System; Vasopressins

Topics: Blood Pressure; Blood Vessels; Diarrhea; Female; Hemorrhage; Humans; Male; Ornithine; Pallor; Postoperative Complications; Skin; Surgical Procedures, Operative; Time Factors; Vasoconstrictor Agents; Vasopressins

Topics: Aminocaproates; Aprotinin; Bilirubin; Blood Proteins; Child; Esophageal and Gastric Varices; Esophagus; Hemorrhage; Humans; Hypertension, Portal; Liver Cirrhosis; Methods; Portacaval Shunt, Surgical; Vasopressins

Topics: Abnormalities, Drug-Induced; Animals; Arteries; Epinephrine; Female; Fetus; Forelimb; Hemorrhage; Hindlimb; Mice; Norepinephrine; Pregnancy; Vasopressins; Veins

Topics: Aminohippuric Acids; Animals; Atrial Function; Blood Pressure; Creatinine; Hematocrit; Hemorrhage; Inulin; Osmolar Concentration; Plasma Volume; Rheology; Sheep; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Acute Kidney Injury; Anesthesia; Blood Pressure; Glomerular Filtration Rate; Hemorrhage; Hepatic Artery; Humans; Hypotension; Kidney; Liver Circulation; Sympathetic Nervous System; Urine; Vascular Resistance; Vasopressins

Topics: Aminohippuric Acids; Animals; Blood Pressure; Diuresis; Dogs; Female; Glomerular Filtration Rate; Hemorrhage; Infusions, Parenteral; Kidney Tubules; Mannitol; Natriuresis; Osmolar Concentration; Potassium; Sodium; Urine; Vascular Resistance; Vasopressins

Topics: Animals; Cerebral Cortex; Cerebral Decortication; Diencephalon; Dogs; Hemorrhage; Hypertonic Solutions; Spinal Cord; Vagotomy; Vagus Nerve; Vasopressins

Topics: Female; Genital Diseases, Female; Hemorrhage; Hemostasis; Hemostatics; Humans; Ornithine; Pregnancy; Tyrosine; Vasopressins

Topics: Animals; Cold Temperature; Electrophoresis, Disc; Female; Growth Hormone; Hemorrhage; Hypothalamus; Insulin; Lactation; Laparotomy; Male; Oxytocin; Physical Exertion; Pituitary Gland; Pregnancy; Rats; Sex Factors; Stress, Physiological; Swimming; Tissue Extracts; Vasopressins

Topics: Animals; Cold Temperature; Electrophoresis, Disc; Female; Hemorrhage; Insulin; Lactation; Laparotomy; Male; Oxytocin; Physical Exertion; Pituitary Gland; Pregnancy; Prolactin; Rats; Stress, Physiological; Swimming; Time Factors; Vasopressins

Topics: Animals; Arteries; Blood Pressure; Blood Volume; Catheterization; Creatinine; Diuresis; Dogs; Glomerular Filtration Rate; Hemorrhage; Heparin; Kidney; Osmolar Concentration; Vasopressins; Veins; Water-Electrolyte Balance

Topics: Animals; Cordotomy; Decerebrate State; Dogs; Female; Hemorrhage; Hypertonic Solutions; Hypothalamo-Hypophyseal System; Male; Pituitary Gland, Posterior; Sodium Chloride; Vagotomy; Vasopressins

Topics: Blood Pressure; Chemical Phenomena; Chemistry; Epinephrine; Felypressin; Female; Gastrointestinal Motility; Hemorrhage; Hemostatics; Humans; Ornithine; Pulse; Time Factors; Vagina; Vasopressins; Wound Healing

Topics: Anesthesia, General; Blood Vessels; Felypressin; Female; Genital Neoplasms, Female; Hemorrhage; Humans; Hysterectomy; Ornithine; Postoperative Care; Preoperative Care; Vasopressins

Topics: Animals; Blood Flow Velocity; Blood Pressure; Cardiac Output; Dogs; Felypressin; Hemorrhage; Hypoxia; Mesenteric Arteries; Mesenteric Veins; Portal Vein; Vasopressins

Topics: Animals; Hemorrhage; Parabiosis; Rats; Secretory Rate; Vasopressins

Topics: Animals; Arginine; Hemorrhage; Metabolic Clearance Rate; Parabiosis; Rats; Time Factors; Vasopressins

Topics: Esophageal and Gastric Varices; Felypressin; Female; Fructose; Hemorrhage; Humans; Injections, Intravenous; Liver Cirrhosis; Male; Vasopressins

Topics: Anesthesia; Animals; Arginine; Blood Proteins; Female; Hemorrhage; Kidney; Metabolic Clearance Rate; Oxytocin; Pentobarbital; Pressure; Protein Binding; Rats; Temperature; Time Factors; Vasopressins

1. The release of vasopressin in response to haemorrhage and the effects of vasopressin infusions on blood pressure and heart rate have been investigated in anaesthetized dogs. Haemorrhage was produced by the method of Lamson & de Türk (1945), which allows for a precise control of the changes in arterial blood pressure.2. Blood samples were collected from an external jugular vein, from a femoral vein or from a femoral artery and extracted with alcohol; blood extracts were assayed for antidiuretic activity.3. Haemorrhage experiments showed that vasopressin secretion is increased when the fall in diastolic blood pressure (diastolic DeltaP) is 25 mm Hg or more. Mild hypotensions (diastolic DeltaP ranging from 21 to 30 mm Hg) produce an average fourfold increase in the concentration of vasopressin in blood. Such increase is maintained throughout the oligaemic period. Severe hypotensions produce, in most cases, a biphasic secretory response, with an initial high peak followed by a lower, constant, secretory plateau. In all experiments, the retransfusion of blood restored vasopressin to control levels.4. Vasopressin infusion experiments showed that the amounts of hormone secreted in response to haemorrhage are sufficient to cause vasopressor response, provided that the buffering action of blood pressure regulation mechanisms is suppressed. It was also found that the amounts of vasopressin secreted in response to haemorrhage are apparently adequate, if the function of such secretion is to combat the hypotension which follows haemorrhage.5. The effect of hypophysectomy on the blood pressure of animals previously submitted to bilateral division of the vagi and sinus nerves (deafferented animals) was also investigated. It was found that hypophysectomy is followed by a fall in arterial blood pressure which is positively correlated to the previous existing amounts of vasopressin. The time course of this hypotension is similar to that following the stopping of an infusion in a deafferented hypophysectomized animal. In some experiments it was shown that, following hypophysectomy, blood pressure can be restored to its pre-hypophysectomy level by an adequate infusion of vasopressin.6. It is proposed that the release of vasopressin in response to stimuli arising from cardiovascular sensory receptors plays a part in the mechanism of blood pressure regulation.

Topics: Animals; Blood Pressure; Carotid Sinus; Dogs; Heart Rate; Hemorrhage; Hypophysectomy; Injections, Intravenous; Reserpine; Vagotomy; Vasopressins

Topics: Animals; Dogs; Hemorrhage; Hypertonic Solutions; Jugular Veins; Sensory Receptor Cells; Vagus Nerve; Vasopressins

Topics: Animals; Arousal; Blood Glucose; Chlorpromazine; Fatty Acids, Nonesterified; Growth Hormone; Haplorhini; Hemorrhage; Histamine; Hypoglycemia; Morphine; Pentobarbital; Vasopressins

1. An investigation has been carried out into various factors which influence the transmucosal potential difference (p.d.) of rat colon in vivo when the p.d. is either high (> 30 mV) or low (< 20 mV).2. The p.d. was uninfluenced by short duration anaesthesia with ether or pentobarbitone. When anaesthesia was prolonged for several hours, p.d. rose steadily. The gradient of p.d. along the descending colon which developed and its elimination by adrenalectomy suggested that the rise was due to increased secretion of adrenal steroids.3. P.d. was increased by Na depletion after a delay of about 18 hr and fell again following Na repletion with a similar time delay. A characteristic gradient of p.d. along the descending colon was seen.4. Both haemorrhage and anoxia caused a rapid fall of p.d. P.d. was restored rapidly to its previous level when anoxia was corrected.5. Vasopressin (I.V.) in low dose was without effect; in high dose it caused a transient fall of p.d. associated with intense vasoconstriction of gut blood vessels.6. The following factors studied were without effect on p.d.: presence of glucose within the lumen; considerable osmotic gradients across the mucosa; variation of luminal pH over the range 5.2-9.8; intravenous administration of acetazolamide, chlorothiazide, frusemide, triamterene, ethacrynic acid or ouabain. Ouabain in the luminal solution also had no effect in all but two rats in which a small fall of p.d. was seen.7. 2,4-dinitrophenol, 10(-2)M, in the lumen caused a small fall of p.d. only if the p.d. was high.8. Experiments were done to determine the effect on p.d. of altering the ionic composition of the luminal solution. When the p.d. was low (< 20 mV) alteration of [Na], [K] or [Cl] produced small absolute changes of the p.d., all of comparable magnitude. The changes could be interpreted as due to diffusion potentials resulting from the ionic gradients across the mucosa. When the p.d. was high (> 30 mV), it showed a striking dependence on the luminal [Na] only, consistent with the presence of a large p.d. due to active Na transport.

Topics: Acetazolamide; Adrenalectomy; Animals; Biological Transport, Active; Blood Vessels; Chlorides; Chlorothiazide; Colon; Dinitrophenols; Electric Conductivity; Electrophysiology; Ethacrynic Acid; Ethyl Ethers; Furosemide; Glucose; Hemorrhage; Hydrogen-Ion Concentration; Hypoxia; Intestinal Mucosa; Ions; Male; Osmosis; Ouabain; Pentobarbital; Potassium; Rats; Sodium; Triamterene; Vasopressins

Topics: Epinephrine; Felypressin; Female; Hemorrhage; Humans; Hysterectomy; Ornithine; Oxytocin; Phenylalanine; Postoperative Complications; Vagina; Vasopressins

Topics: Animals; Biological Assay; Diuresis; Female; Hemorrhage; Mammary Glands, Animal; Oxytocin; Pituitary Gland, Posterior; Rats; Vasopressins

Topics: Animals; Arginine; Body Fluids; Dogs; Extracellular Space; Hemorrhage; Natriuresis; Oxytocin; Vasopressins

Topics: Animals; Arteries; Biological Assay; Blood-Brain Barrier; Cisterna Magna; Diuresis; Dogs; Female; Hemorrhage; Homeostasis; Male; Neurosecretion; Rabbits; Vasopressins

Topics: Animals; Calcium Chloride; Chlorpheniramine; Chlorpromazine; Electric Stimulation; Epinephrine; Hemorrhage; Hexamethonium Compounds; Male; Mecamylamine; Norepinephrine; Pempidine; Phenothiazines; Pituitary Gland, Posterior; Promethazine; Rats; Reserpine; Tyramine; Vagus Nerve; Vasopressins

Topics: Acetylcholine; Animals; Calcium Chloride; Carbachol; Electric Stimulation; Female; Guinea Pigs; Hemorrhage; Jugular Veins; Lactation; Male; Oxytocin; Pituitary Gland, Posterior; Pregnancy; Rats; Sodium Chloride; Vagus Nerve; Vasopressins

Topics: Animals; Dogs; Hemorrhage; Injections, Intravenous; Isotonic Solutions; Natriuresis; Oxytocin; Sodium; Sodium Chloride; Vasopressins

Topics: Animals; Blood Pressure; Carotid Body; Denervation; Dogs; Heart Rate; Hemorrhage; Male; Pressoreceptors; Pulse; Vagotomy; Vagus Nerve; Vasopressins

Topics: Animals; Antidiuretic Agents; Cats; Female; Femoral Artery; Femoral Vein; Hemorrhage; Jugular Veins; Monophenol Monooxygenase; Oxytocin; Vagus Nerve Stimulation; Vasopressins

Topics: Animals; Barium; Calcium; Dogs; Hemorrhage; Hypotension; Hypothalamo-Hypophyseal System; In Vitro Techniques; Male; Microscopy, Electron; Neurosecretion; Pituitary Gland, Posterior; Potassium; Vasopressins

Topics: Animals; Diuresis; Dogs; Hemorrhage; Monitoring, Physiologic; Pain; Vasopressins; Wounds and Injuries

1. The release of neurohypophysial hormones in response to carotid occlusion and haemorrhage has been studied in anaesthetized cats. Samples of jugular venous blood were extracted with alcohol and the extracts assayed for antidiuretic and milk-ejecting activity.2. The release of vasopressin in response to bilateral occlusion of the common carotid arteries has been confirmed in the cat; this effect was abolished when the sinus nerves were divided.3. Using a new sensitive preparation for the assay of milk-ejecting activity in blood extracts, it has been shown that no oxytocin accompanies the release of vasopressin during carotid occlusion.4. The independent release of vasopressin without oxytocin during haemorrhage has also been confirmed, and the role of the sinus nerves and vagi in this response investigated. Bilateral division of either nerve reduced the response, but the vagus appeared to be of greater importance than the sinus nerve.5. A reflex arc for the selective release of vasopressin has been proposed, of which the fibres of the sinus nerves and vagi form the afferent component and the neurones of the supraoptic nucleus the efferent component.

Topics: Animals; Carotid Arteries; Carotid Body; Carotid Sinus; Cats; Female; Hemorrhage; Oxytocin; Pressoreceptors; Rats; Reflex; Sympathectomy; Vagotomy; Vagus Nerve; Vasopressins

Topics: Animals; Blood Pressure; Carotid Sinus; Dogs; Hemorrhage; Male; Perfusion; Pituitary Gland, Posterior; Pressoreceptors; Sensory Receptor Cells; Vagotomy; Vasopressins

Topics: Animals; Cerebral Cortex; Diencephalon; Dogs; Electric Stimulation; Hemorrhage; Hypertonic Solutions; Nicotine; Sodium Chloride; Vasopressins

Topics: Anesthesia; Animals; Diuresis; Ethanol; Hemorrhage; Hypophysectomy; Male; Osmosis; Pain; Rats; Vasopressins

Topics: Anesthesia; Animals; Ethyl Ethers; Hemorrhage; Microscopy, Electron; Neurosecretion; Oxytocin; Pituitary Gland, Posterior; Rats; Vasopressins

Topics: Animals; Blood Pressure; Dogs; Hemorrhage; Hypertension, Portal; Portography; Vasopressins

Topics: Angiography; Animals; Aortography; Blood Circulation; Dogs; Esophageal and Gastric Varices; Hemorrhage; Hemostasis; Hypertension, Portal; Vasopressins

Topics: Animals; Biological Assay; Calcium Chloride; Hemorrhage; Hypertonic Solutions; Male; Rats; Vagus Nerve; Vasopressins

Topics: Female; Hemorrhage; Hemostasis; Humans; Male; Postoperative Complications; Prostatectomy; Urethra; Urinary Bladder Diseases; Urinary Bladder Neoplasms; Vasopressins

Topics: Animals; Aortic Diseases; Atropine; Dogs; Electrocardiography; Epinephrine; Heart Auscultation; Heart Sounds; Hemodynamics; Hemorrhage; Histamine; Infusions, Parenteral; Isoproterenol; Methoxamine; Myocardial Infarction; Norepinephrine; Pharmacology; Phenylephrine; Phonocardiography; Pulmonary Artery; Research; Respiration; Vascular Diseases; Vasopressins; Venae Cavae; Veratrine

Topics: Arginine Vasopressin; Child; Cleft Palate; Epinephrine; Felypressin; Hemorrhage; Hemostatics; Humans; Infant; Pharmacology; Surgery, Oral; Vasopressins

Topics: Blood Transfusion; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Hemorrhage; Humans; Hypertension; Hypertension, Portal; Liver Cirrhosis; Mortality; Omentum; Splenectomy; Surgical Procedures, Operative; Vasopressins

Topics: Adrenal Glands; Adrenocorticotropic Hormone; Animals; Dogs; Hemorrhage; Hypotension; Kidney; Rubidium; Thyroid Gland; Vasopressins

Topics: Arginine Vasopressin; Blood; Blood Volume; Carotid Arteries; Creatine; Creatinine; Diuresis; Growth; Hemorrhage; Rats; Research; Urine; Vasopressins

Topics: Arginine Vasopressin; Esophageal and Gastric Varices; Felypressin; Gastrointestinal Hemorrhage; Hemorrhage; Humans; Vasopressins

Topics: Acute Kidney Injury; Atropine; Biomedical Research; Blood Volume; Convalescence; Dehydration; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Edema; Epinephrine; Female; Heart Failure; Hemorrhage; Humans; Hypertonic Solutions; Menstruation; Pharmacology; Placebos; Pregnancy; Renal Insufficiency; Salivation; Sweating; Uremia; Vasopressins; Water-Electrolyte Balance

Topics: Blood Volume; Creatine; Creatinine; Dehydration; Diuresis; Dogs; Hemorrhage; Hypertonic Solutions; Kidney Tubules; Mannitol; Natriuresis; Osmosis; Pharmacology; Photometry; Potassium; Research; Urine; Vasopressins; Water-Electrolyte Balance

Topics: Anesthesia; Anesthesia, Local; Anesthesiology; Angiotensins; Blood Vessels; Epinephrine; Hemorrhage; Humans; Mephentermine; Metaraminol; Methoxamine; Norepinephrine; Pharmacology; Phenylalanine; Phenylephrine; Pilot Projects; Skin; Skin Transplantation; Vasoconstrictor Agents; Vasopressins

Topics: Arginine Vasopressin; Hemodynamics; Hemorrhage; Humans; Portal System; Vasopressins

Topics: Biomedical Research; Female; Gynecologic Surgical Procedures; Gynecology; Hemorrhage; Humans; Vasopressins

Topics: Arginine Vasopressin; Hemorrhage; Vasopressins

Topics: Esophageal and Gastric Varices; Hemorrhage; Humans; Vasopressins

Topics: Adrenal Glands; Animals; Blood; Hemorrhage; Hormones; Pituitary Gland; Pituitary Gland, Posterior; Rats; Vasopressins

Topics: Arginine Vasopressin; Female; Hemorrhage; Humans; Uterine Hemorrhage; Uterus; Vasopressins

Topics: Arginine Vasopressin; Female; Genital Diseases, Female; Hemorrhage; Humans; Pituitary Gland; Pituitary Hormones; Uterine Hemorrhage; Uterus; Vasopressins