pituitrin and Tachycardia

Vasopressin is a 9-amino acid peptide synthesized by magnocellular neurons of the hypothalamus and released from posterior pituitary gland. The primary physiological role of vasopressin is the maintenance of fluid homeostasis. In this review, the classification of vasopressin receptors, namely V1 vascular, V2 renal, V3 pituitary, oxytocin receptors, and purinergic receptors, and the effects of vasopressin on vascular smooth muscles, the heart, and the kidneys are discussed. Mortality rates of vasodilatory (or distributive), for example septic shock, are high. The use of vasopressin is an alternative therapy for vasodilatory shock with better outcome. Vasopressin is effective in resuscitation of adults after ventricular fibrillation or pulseless tachycardia, when epinephrine is not effective.

Topics: Adult; Clinical Trials as Topic; Dilatation, Pathologic; Heart; Heart Arrest; Homeostasis; Humans; Intensive Care Units; Kidney; Muscle, Smooth, Vascular; Receptors, Vasopressin; Resuscitation; Shock; Shock, Septic; Survival Analysis; Tachycardia; Time Factors; Treatment Outcome; Vasoconstrictor Agents; Vasodilation; Vasopressins; Ventricular Fibrillation

Topics: Adrenergic alpha-Agonists; Adrenergic beta-Agonists; Advanced Cardiac Life Support; Algorithms; Anti-Arrhythmia Agents; Bicarbonates; Bradycardia; Calcium Channel Blockers; Cardiac Pacing, Artificial; Cardiotonic Agents; Dobutamine; Dopamine; Electric Countershock; Electrocardiography; Epinephrine; Heart Arrest; Humans; Injections, Intravenous; Isoproterenol; Sympathomimetics; Tachycardia; Vasoconstrictor Agents; Vasopressins; Ventricular Fibrillation; Verapamil

The atrial natriuretic peptide (ANP) is rapidly secreted in case of acute changes in atrial volume and heart rate. Its effects are mainly natriuretic and vasodilator. This hormone is of interest to the anaesthetist because induction of anaesthesia, epidural anaesthesia and administration of morphine all result in changes in ANP plasma concentration.

Topics: Anesthesia; Atrial Natriuretic Factor; Extracorporeal Circulation; Heart; Humans; Kidney; Morphine; Plasma Volume; Receptors, Opioid; Tachycardia; Vasopressins

Although ANF research started 30 years ago, the atrial natriuretic factor (ANF) was only discovered recently (1981). The presence of such a factor has been suspected for many years because of histological and physiological arguments. In 1956, Kish found "dense granules" in the atrial walls of guinea pigs. Gauer and Henry could explain some of their experimental results on diuresis and natriuresis only by suggesting the presence of a third hormonal factor, but neither by the renin-angiotensin system, nor the anti-diuretic hormone. Hall et al. were the first to recognize a link between the granules and water and sodium metabolism. But it was De Bold who published the crucial experiment in 1981: injecting right atrial extracts to anaesthetized rats rapidly induced intense and transitory diuresis and natriuresis. ANF was born, and, at the same time, the concept of the heart as an endocrine gland. Indeed, ANF corresponds to the strict definition of a hormone. It has the following properties: natriuresis and diuresis via an increase in glomerular filtration fraction without any major changes in renal plasma flow; direct vasodilation of the large arteries with only few effects on small arterioles and veins. The stimuli for ANF secretion are mechanical and pharmacological, especially drugs currently used by anaesthetists. Atrial distension is the main mechanical stimulus. An increase in atrial transmural pressure is always followed by a release in ANF, but this effect is not constant for increases in intra-luminal pressure. It is the former pressure gradient alone that reflects the volume of the right atrium, the mechanical stimulus for ANF secretion. Tachycardia, or, more precisely, an increase in the atrial contraction rate, also leads to an important release of ANF. Cardiac nerves are not necessary for this, as demonstrated by studies in heart transplant patients. Only few pharmacological agents have been shown to really stimulate ANF secretion. In rats, morphine has a direct secretory effect, whereas ketamine hydrochloride, diethylether and chloral hydrate do so by increasing the release of catecholamines. The effects of alpha, beta adrenergic agonists and calcium agonists remain controversial. ANF, which has diuretic and vasodilator effects, plays a part, together with the renin-angiotensin system and the anti-diuretic hormone, in blood volume control in mammals. However, it has a special role to play, because it is a rapid release hormone: rapid vascular fi

Topics: Anesthetics; Animals; Atrial Natriuretic Factor; Calcium Channel Agonists; Cardiomegaly; Diuresis; Fentanyl; Glomerular Filtration Rate; Humans; Rats; Renin-Angiotensin System; Sympathetic Nervous System; Sympathomimetics; Tachycardia; Vasodilation; Vasopressins

Various rhythm disturbances occur in the postoperative patient. Proper management requires an awareness of clinical circumstances in which they are most likely to happen. Often, the appearance of new arrhythmias in the postoperative period is a manifestation of underlying remediable medical problems. Direct antiarrhythmic therapy is unnecessary in many patients when these precipitating conditions are properly treated.

Topics: Arrhythmias, Cardiac; Atrial Fibrillation; Atrial Flutter; Bradycardia; Bundle-Branch Block; Electrocardiography; Heart Diseases; Humans; Surgical Procedures, Operative; Tachycardia; Tachycardia, Paroxysmal; Vasopressins

Topics: Aldosterone; Angiotensins; Autonomic Nervous System; Autonomic Nervous System Diseases; Desoxycorticosterone; Ephedrine; Fludrocortisone; Humans; Hypotension, Orthostatic; Posture; Sweating; Tachycardia; Vasopressins

Although the use of opioids during general anaesthesia suppresses stress response to surgery and pain, the effects on antidiuretic hormone (ADH) are controversial. The aim of this study was to find the effects of morphine with either intravenous infusion or epidural route on ADH and other stress hormones.. Fifty children aging (1-15 years) undergoing major genito-urinary or abdominal operations were included in this study. The patients were allocated randomly to two groups receiving either a single dose of epidural morphine 0.1 mg.kg-1 (EP group, n = 25) postinduction or morphine infusion (INF group; n = 25) at 0.02 mg.kg-1.h-1 following 0.05 mg.kg-1 bolus. Blood samples were withdrawn for plasma ADH, osmolality, glucose, cortisol, insulin and morphine level analysis following induction and 1, 5, 12 and 24 h after initial morphine administration.. The two groups were similar in demographic factors, pain scores, sedation scores, and incidence of nausea and vomiting. The amount of morphine received was different between groups and the changes in serum levels of morphine were statistically significant in EP group ( P < 0.05). The changes in cortisol, blood glucose and insulin levels were insignificant in both groups (P > 0.05). The changes of ADH levels were significant at time-points in both groups, reaching control levels at the 24th hour (P < 0.05).. Despite the effective pain therapy and suppression of cortisol and insulin response to surgical stimulus, the increase in ADH secretion is not effected by systemic or epidural morphine administration.

Topics: Abdomen; Adolescent; Analgesia, Epidural; Analgesics, Opioid; Blood Glucose; Child; Child, Preschool; Female; Hormones; Humans; Hydrocortisone; Infant; Infusions, Intravenous; Insulin; Male; Morphine; Pain Measurement; Pain, Postoperative; Surgical Procedures, Operative; Tachycardia; Urogenital Surgical Procedures; Vasopressins

Cardiovascular and hormonal responses to reconstructive abdominal aortic surgery were studied in 20 patients anaesthetized either with moderate-dose fentanyl (20 micrograms kg-1) combined with isoflurane, nitrous oxide and oxygen (n = 10), or with thoracolumbar epidural bupivacaine combined with isoflurane, nitrous oxide and oxygen (n = 10). After the start of operation, hypotension occurred in four patients in the epidural group. In both groups, the aortic cross-clamping caused slight increases both in mean arterial pressure and in calculated systemic vascular resistance, and a significant decrease in cardiac index. At the same time, a marked increase in plasma vasopressin was seen in the fentanyl group. Plasma catecholamines were low in both groups. After aortic declamping, the cardiac index improved in both groups, although two patients in the fentanyl group and four patients in the epidural group were hypotensive. Post-operatively, eight patients in the fentanyl group were hypertensive, versus none in the epidural group, in which bupivacaine-fentanyl was administered epidurally. At the same time, plasma vasopressin and adrenaline increased significantly in both groups, whereas plasma noradrenaline did so only in the fentanyl group. The results suggest that thoracolumbar epidural bupivacaine combined with low-dose isoflurane in nitrous-oxide-oxygen prevents intra-operative hypertension and tachycardia, but it may cause hypotension. Post-operative hypertension and tachycardia as well as the increase in plasma noradrenaline are prevented by epidural administration of bupivacaine-fentanyl.

Topics: Aged; Anesthesia, Epidural; Anesthesia, Inhalation; Anesthesia, Intravenous; Aorta, Abdominal; Blood Pressure; Bupivacaine; Cardiac Output; Female; Fentanyl; Fluid Therapy; Heart Rate; Humans; Hypertension; Hypotension; Intraoperative Complications; Isoflurane; Male; Middle Aged; Norepinephrine; Pain, Postoperative; Postoperative Complications; Tachycardia; Vascular Resistance; Vasopressins

Topics: Adult; Analysis of Variance; Blood Pressure; Clinical Trials as Topic; Computers; Ethinyl Estradiol; Fluoxymesterone; Follicle Stimulating Hormone; Humans; Luteinizing Hormone; Male; Oxytocin; Radioimmunoassay; Tachycardia; Vasopressins

Topics: Adrenergic beta-Antagonists; Amputation, Surgical; Cefepime; Child; Clindamycin; Debridement; Diagnosis, Differential; Epinephrine; Fasciotomy; Female; Fluid Therapy; Humans; Hypertension; Ischemia; Leg; Norepinephrine; Propranolol; Shock, Septic; Tachycardia; Therapeutic Irrigation; Treatment Outcome; Vasopressins

Restraint stress (RS) is an unavoidable stress model that triggers activation of the autonomic nervous system, endocrine activity, and behavioral changes in rodents. Furthermore, RS induces secretion of oxytocin into the bloodstream, indicating a possible physiological role in the stress response in this model. The presence of oxytocin receptors in vessels and heart favors this possible idea. However, the role of oxytocin secreted in RS and effects on the cardiovascular system are still unclear. The aim of this study was to analyze the influence of oxytocin on cardiovascular effects during RS sessions. Rats were subjected to pharmacological (blockade of either oxytocin, vasopressin, or muscarinic receptors) or surgical (hypophysectomy or sinoaortic denervation) approaches to study the functional role of oxytocin and its receptor during RS. Plasma levels of oxytocin and vasopressin were measured after RS. RS increased arterial pressure, heart rate, and plasma oxytocin content, but not vasopressin. Treatment with atosiban (a Gi biased agonist) inhibited restraint-evoked tachycardia without affecting blood pressure. However, this effect was no longer observed after sinoaortic denervation, homatropine (M2 muscarinic antagonist) treatment or hypophysectomy, indicating that parasympathetic activation mediated by oxytocin secreted to the periphery is responsible for blocking the increase in tachycardic responses observed in the atosiban-treated group. Corroborating this, L-368,899 (oxytocin antagonist) treatment showed an opposite effect to atosiban, increasing tachycardic responses to restraint. Thus, this provides evidence that oxytocin secreted to the periphery attenuates tachycardic responses evoked by restraint via increased parasympathetic activity, promoting cardioprotection by reducing the stress-evoked heart rate increase.

Topics: Animals; Antidiuretic Hormone Receptor Antagonists; Baroreflex; Blood Pressure; Heart Rate; Male; Muscarinic Agonists; Oxytocin; Parasympatholytics; Rats, Wistar; Receptor, Muscarinic M2; Receptors, Vasopressin; Restraint, Physical; Stress, Psychological; Tachycardia; Tropanes; Vasopressins; Vasotocin

Topics: Acidosis, Lactic; Acute Disease; Administration, Intravenous; Adult; Aged; Alcoholism; Anti-Bacterial Agents; Bicarbonates; Comorbidity; Confusion; Glasgow Coma Scale; Humans; Hyperlactatemia; Hypotension; Intubation, Intratracheal; Male; Norepinephrine; Respiration, Artificial; Respiratory Insufficiency; Tachycardia; Thiamine; Vasoconstrictor Agents; Vasopressins; Vitamin B Complex

It is well recognized that vasopressin modulates the neurogenic control of the circulation. Here, we report the central mechanisms by which vasopressin modulates cardiovascular response to stress induced by immobilization.. Experiments were performed in conscious male Wistar rats equipped with radiotelemetric device for continuous measurement of haemodynamic parameters: systolic and diastolic BP and heart rate (HR). The functioning of the spontaneous baro-receptor reflex (BRR) was evaluated using the sequence method and the following parameters were evaluated: BRR sensitivity (BRS) and BRR effectiveness index (BEI).. Under baseline physiological conditions intracerebroventricular injection of 100 and 500 ng of selective non-peptide V1a or V1b or V2 receptor antagonist did not modify BP, HR and BRR. Rats exposed to 15 min long stress by immobilization exhibited increase of BP, HR, reduction of BRS and no change in BEI. Pretreatment of rats with V1a receptor antagonist did not modulate the BP, HR, BRS and BEI response to stress. Pretreatment of rats with V1b receptor and V2 receptor antagonist, at both doses, prevented BRR desensitization and tachycardia, but failed to modulate stress-induced hypertension.. Vasopressin by the stimulation of central V1b- and V2-like receptors mediates stress-induced tachycardia and BRR desensitization. If these mechanisms are involved, BRR desensitization in heart failure and hypertension associated with poor outcome, they could be considered as novel targets for cardiovascular drug development.

Topics: Allostasis; Animals; Anti-Anxiety Agents; Antidiuretic Hormone Receptor Antagonists; Baroreflex; Cerebral Ventricles; Disease Models, Animal; Dose-Response Relationship, Drug; Hypertension; Injections, Intraventricular; Male; Nerve Tissue Proteins; Neurons; Pilot Projects; Random Allocation; Rats; Rats, Wistar; Receptors, Vasopressin; Restraint, Physical; Stress, Physiological; Stress, Psychological; Tachycardia; Vasopressins

The Vav family is a group of signal transduction molecules that activate Rho/Rac GTPases during cell signaling. Experiments using knockout mice have indicated that the three Vav proteins present in mammals (Vav1, Vav2, and Vav3) are essential for proper signaling responses in hematopoietic cells. However, Vav2 and Vav3 are also highly expressed in nonhematopoietic tissues, suggesting that they may have additional functions outside blood cells. Here, we report that this is the case for Vav2, because the disruption of its locus in mice causes tachycardia, hypertension, and defects in the heart, arterial walls, and kidneys. We also provide physiological and pharmacological evidence demonstrating that the hypertensive condition of Vav2-deficient mice is due to a chronic stimulation of the renin/angiotensin II and sympathetic nervous systems. Together, these results indicate that Vav2 plays crucial roles in the maintenance of cardiovascular homeostasis in mice.

Topics: Adrenal Glands; Aldosterone; Animals; Aorta; Endothelins; Gene Expression Regulation; Guanine Nucleotide Exchange Factors; Heart Ventricles; Hypertension; Kidney; Kidney Function Tests; Mice; Mice, Knockout; Phenotype; Proto-Oncogene Proteins c-vav; Renin-Angiotensin System; Sympathetic Nervous System; Tachycardia; Vasopressins

We report the case of a 65-year-old man who developed norepinephrine-resistant vasoplegic syndrome after elective off-pump coronary artery bypass surgery (OPCAB). The failure of norepinephrine to improve the patient's hemodynamics prompted us to start treatment with vasopressin; within 30 minutes, the hemodynamics began to improve. After 12 hours, the patient was stable enough to be weaned from the vasopressin. He was discharged from the hospital on the 10th postoperative day. To our knowledge, ours is the 1st report of vasopressin use for vasodilatory shock after OPCAB in the English-language medical literature. Herein, we discuss the pathophysiology and management of vasoplegic syndrome--which is controversial--with special emphasis on the use of vasopressin in this situation.

Topics: Aged; Blood Pressure; Cardiac Output, High; Coronary Artery Bypass, Off-Pump; Humans; Hypotension; Male; Syndrome; Tachycardia; Vascular Resistance; Vasoconstrictor Agents; Vasopressins

The cardiovascular effects of intracerebroventricular (i.c.v.) administration of choline were studied in endotoxin-treated rats. Intravenous (i.v.) endotoxin (20 mg/kg) caused a moderate hypotension and tachycardia within 10 min of treatment. Choline (50, 100, and 150 microg; i.c.v.) increased blood pressure and decreased heart rate in this condition in a dose-dependent manner. Mecamylamine (50 microg; i.c.v.) pretreatment prevented the pressor and bradycardic responses to choline, whereas atropine (10 microg; i.c.v.) failed to alter both responses. Atropine pretreatment, alone, inhibited endotoxin-induced hypotension. The pressor responses to choline in endotoxin-treated rats were attenuated by pretreatment with hemicholinium-3 (20 microg; i.c.v.), a high-affinity neuronal choline-uptake inhibitor. Plasma vasopressin levels of endotoxin-treated rats were severalfold higher than those of control animals, and choline (50-150 microg; i.c.v.) produced further increases in plasma vasopressin in this condition. Mecamylamine abolished vasopressin response to endotoxin as well as to choline. The vasopressin receptor antagonist, (beta-mercapto-beta,beta-cyclopentamethylene-propionyl(1)-O-Me-Tyr2,Arg8 )-vasopressin (10 microg/kg; i.v.) administered 5 min after choline decreased blood pressure from the increased level to the precholine levels but did not alter bradycardia. These results indicate that, in rats treated with endotoxin, choline increases blood pressure and decreases heart rate by a presynaptic mechanism leading to the activation of central nicotinic cholinergic pathways. An increase in plasma vasopressin levels seems to be involved in the pressor, but not in the bradycardic response, to choline.

Topics: Animals; Blood Pressure; Choline; Cholinergic Agents; Dose-Response Relationship, Drug; Endotoxins; Heart Rate; Hormone Antagonists; Hypotension; Injections, Intravenous; Injections, Intraventricular; Male; Muscarinic Antagonists; Nicotinic Antagonists; Rats; Rats, Wistar; Shock, Septic; Tachycardia; Vasopressins

To address the role of oxytocin in the control of cardiovascular reactivity, we examined the effect of central injection of oxytocin, vasopressin and mixed base antisense oligodeoxynucleotides on stress-induced cardiovascular and endocrine changes. Antisense oligomers were injected into the paraventricular nucleus (PVN), 4 h prior to the stress test. The oxytocin antisense abolished the tachycardia produced by 5 min of shaker stress. The blood pressure and plasma oxytocin responses were not different between the groups. PVN levels of OT were reduced in the oxytocin antisense-treated group while brain stem levels were increased. These results demonstrate the importance of a specific peptide system, the PVN/oxytocin axis, in stress-induced tachycardia. Further, the data illustrate the effectiveness of short-term treatment with antisense oligomers on physiological responses.

Topics: Animals; Base Sequence; Brain; Male; Molecular Sequence Data; Oligonucleotides, Antisense; Oxytocin; Paraventricular Hypothalamic Nucleus; Rats; Rats, Sprague-Dawley; Stress, Physiological; Tachycardia; Vasopressins

1. Male, Long Evans rats were chronically instrumented with pulsed Doppler flow probes and intravascular catheters to permit assessment of the regional haemodynamic responses to human and rat adrenomedullin, to compare the responses to human adrenomedullin to those of human alpha-CGRP in the absence and presence of the CGRP1-receptor antagonist, human alpha-CGRP [8-37], and to determine the involvement of nitric oxide (NO)-mediated mechanisms in the responses to human adrenomedullin, relative to human alpha-CGRP. 2. Human and rat adrenomedullin (0.3, 1, and 3 nmol kg-1, i.v.) caused dose-dependent hypotension and tachycardia, accompanied by increases in renal, mesenteric and hindquarters flows and vascular conductances. At the lowest dose only, the hypotensive and mesenteric vasodilator effects of rat adrenomedullin were significantly greater than those of human adrenomedullin. 3. Human alpha-CGRP at a dose of 1 nmol kg-1 caused hypotension, tachycardia and increases in hindquarters flow and vascular conductance, but reduction in renal and mesenteric flows, and only transient vasodilatations in these vascular beds. These effects were substantially inhibited by human alpha-CGRP [8-37] (100 nmol kg-1 min-1), but those of human adrenomedullin (1 nmol kg-1) were not; indeed, the mesenteric haemodynamic effects of the latter peptide were enhanced by the CGRP1-receptor antagonist. 4. In the presence of the NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 183 nmol kg-1 min-1), there was only a slight, but significant, inhibition of the hindquarters hyperaemic vasodilator effect of human adrenomedullin, but not that of human alpha-CGRP. 5. These results indicate that the marked regional vasodilator effects of human (and rat) adrenomedullin are largely independent of NO and, in vivo, do not involve CGRP1-receptors.

Topics: Adrenomedullin; Angiotensin II; Animals; Antihypertensive Agents; Arginine; Blood Pressure; Calcitonin Gene-Related Peptide; Catheterization, Peripheral; Dose-Response Relationship, Drug; Heart Rate; Hemodynamics; Humans; Hypertension; Hypotension; Laser-Doppler Flowmetry; Male; NG-Nitroarginine Methyl Ester; Nitric Oxide; Peptide Fragments; Peptides; Random Allocation; Rats; Regional Blood Flow; Renal Circulation; Tachycardia; Vasopressins

Vasopressin (VP) levels were evaluated by radioimmunoassay (RIA) in the arterial (A), peripheral (Vp) and jugular (Vj) vein blood and in CSF in 102 patients with brain tumors. In 60 cases the patients' state was complicated by brain edema (BE) and hemodynamic disturbances (HDD). The obtained data revealed significantly higher VP levels: 1) in A, Vp and CSF in patients with BE (Group A) in comparison with patients without BE (Group B), 2) in Vj in patients with HDD only (Group Bc) and 3) in Vp in patients with HDD and BE (Group Ac) in comparison with Group Bc (p < 0.05). There were marked extremely high VP levels in Vj in patients with severe haemorrhage, tachycardia and high blood pressure (BP) and in CSF in patients with tachycardia, high BP and cardiac arrest (p < 0.05 correspondingly in each of the cases). Our results on a clinical basis confirmed CSF VP influence on BE development. We also confirmed the neurohumoral (through blood) and neurotransmitter (possibly through CSF and/or vasopressinergic pathways) VP influences on cardiovascular regulation mechanisms. We content that this is a pathogenetic basis for application of VP direct or indirect antagonists for preventing and treating brain edema in neurosurgical patients.

Topics: Adolescent; Adult; Aged; Blood-Brain Barrier; Brain Edema; Brain Neoplasms; Cerebral Hemorrhage; Child; Child, Preschool; Female; Heart Arrest; Hemodynamics; Humans; Hypertension; Male; Middle Aged; Postoperative Complications; Radioimmunoassay; Synaptic Transmission; Tachycardia; Vasopressins

The study of renin-angiotensin-aldosterone (RAA) and vasopressin (VP) systems in neurosurgical patients with brain tumors and brain edema (BE) had revealed an excessive activity of these systems with secondary hyperaldosteronism especially with BE that proves the pathogenetic role of these systems. Measurement of Aldosterone (Ald) in CSF may serve as a diagnostic test to help manage the patient's clinical condition. Mechanisms of Ald penetration in CSF assumed to be the result of blood-brain-barrier (BBB) destruction (especially in astrocytomas) and/or the mediation by neuropeptides (for example increasing activity of VP V1-receptors). Results serve as a basis for application of the neuropeptide and hormone antagonists and inhibitors on all stages of cascade reactions taking part in the water and sodium retention.

Topics: Adolescent; Adult; Aged; Aldosterone; Astrocytoma; Blood-Brain Barrier; Brain Edema; Brain Neoplasms; Cerebral Hemorrhage; Child; Child, Preschool; Female; Heart Arrest; Hemodynamics; Humans; Hyperaldosteronism; Hypertension; Male; Middle Aged; Postoperative Complications; Prognosis; Radioimmunoassay; Renin-Angiotensin System; Tachycardia; Vasopressins

Topics: Aged; Aldosterone; Atrial Natriuretic Factor; Cardiac Pacing, Artificial; Coronary Disease; Electrophysiology; Female; Hemodynamics; Humans; Hydrocortisone; Male; Middle Aged; Norepinephrine; Renin; Tachycardia; Vasopressins

A patient experienced hypertension, bradycardia, QT prolongation, and multiple episodes of torsade de pointes while receiving an iv vasopressin infusion. The dysrhythmias were attributed to vasopressin, but may have been potentiated by hypomagnesemia. Upon vasopressin discontinuation, ECG findings returned to normal before magnesium supplementation. Vasopressin may contribute to the development of torsade de pointes.

Topics: Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Humans; Male; Middle Aged; Tachycardia; Vasopressins

Rats subjected to various levels of +Gz acceleration exhibited an increased blood concentration of noradrenalin and adrenalin, indicative of a sympatho-adrenergic reaction. Under the same conditions, from plasma determinations, and by histochemical examination of the supra-optic nucleus, an increased antidiuretic response was noted. This response was reduced in cold environment.

Topics: Animals; Bradycardia; Centrifugation; Cold Temperature; Epinephrine; Heart Rate; Hypergravity; Male; Noise; Norepinephrine; Rats; Rats, Wistar; Supraoptic Nucleus; Tachycardia; 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

Left atrial pacing was performed in three groups of anesthetized dogs. In the first group of eight intact dogs a mean increase in atrial rate (AR) from 140 +/- 7 to 244 +/- 6 was associated with a decrease in urinary osmolality (U osmol) from 631 +/- 72 to 264 +/- 43 mosmol/kg (P less than .001), and free-water clearance (CH20) increased from -.325 +/- .06 to +.355 +/- .15 ml/min (P less than .001). At the same time left atrial pressure (LAP) increased from 6 +/- 1 to 15 +/- 1 mmHg (P less than .001). A second group of studies was performed in six hypophysectomized, steroid-replaced animals receiving 40-50 muU/kg per min of antidiuretic hormone (ADH). In these animals AR was increased from 148 +/- 17 to 250 +/- 17 but diuresis did not occur. In these studies Uosmol was 690 +/- 55 before and 704 +/- 49 mosmol/kg after atrial pacing and CH20 also did not change. Left atrial pressure increased from 10 +/- 2 to 19 +/- 2 mmHg during atrial pacing. A third group of studies was performed in five animals with bilateral cervical vagotomy. In these animals AR was increased from 159 +/- 6 to 258 +/- 17 and LAP increased from 7 +/- 1 to 16 +/- 2 mmHg. Osmolality increased from 808 +/- 72 to 1,049 +/- 65 musmol/kg (P less than .005) and CH20 was unchanged. These results, therefore, indicate that atrial tachycardia primarily increases renal water excretion by suppressing ADH release. This reflex is dependent on the integrity of cervical vagal pathways.

Topics: Animals; Diuresis; Dogs; Female; Hypophysectomy; Kidney; Kidney Concentrating Ability; Male; Tachycardia; Vagotomy; Vagus Nerve; Vasopressins

Topics: Blood Pressure; Heart Atria; Humans; Middle Aged; Tachycardia; Vasopressins

Topics: Aconitum; Amides; Animals; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Asphyxia; Barium; Calcium Chloride; Cardiac Complexes, Premature; Chlorides; Depression, Chemical; Electrocardiography; Guinea Pigs; Heart Rate; Magnesium; Male; Potassium Chloride; Quinidine; Rats; Strophanthins; Tachycardia; Vasopressins; Ventricular Fibrillation

Topics: Adult; Anesthesia, Dental; Humans; Hyperventilation; Male; Prilocaine; Smoking; Syncope; Tachycardia; Tranylcypromine; Vasopressins

Topics: Anesthetics, Local; Blood Pressure; Epinephrine; Felypressin; Hemostasis; Humans; Ischemia; Nausea; Otorhinolaryngologic Diseases; Oxytocin; Pulse; Tachycardia; Vasoconstrictor Agents; Vasopressins

Topics: Emergencies; Heart Arrest; Heart Massage; Histamine H1 Antagonists; Humans; Hypotension; Infusions, Parenteral; Podiatry; Seizures; Spasm; Tachycardia; Vasopressins; Vocal Cord Paralysis