pituitrin and Hypovolemia

Severe trauma constitutes a major cause of death and disability, especially in younger patients. The cerebral autoregulatory capacity only protects the brain to a certain extent in states of hypovolemia; thereafter, neurological deficits and apoptosis occurs. We therefore set out to investigate neuroprotective strategies during haemorrhagic shock. This review was performed in accordance to the PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines. Before the start of the search, a review protocol was entered into the PROSPERO database. A systematic literature search of Pubmed, Web of Science and CENTRAL was performed in August 2017. Results were screened and evaluated by two researchers based on a previously prepared inclusion protocol. Risk of bias was determined by use of SYRCLE's risk of bias tool. The retrieved results were qualitatively analysed. Of 9093 results, 119 were assessed in full-text form, 16 of them ultimately adhered to the inclusion criteria and were qualitatively analyzed. We identified three subsets of results: (1) hypothermia; (2) fluid therapy and/or vasopressors; and (3) other neuroprotective strategies (piracetam, NHE1-inhibition, aprotinin, human mesenchymal stem cells, remote ischemic preconditioning and sevoflurane). Overall, risk of bias according to SYRCLE's tool was medium; generally, animal experimental models require more rigorous adherence to the reporting of bias-free study design (randomization, etc.). While the individual study results are promising, the retrieved neuroprotective strategies have to be evaluated within the current scientific context-by doing so, it becomes clear that specific promising neuroprotective strategies during states of haemorrhagic shock remain sparse. This important topic therefore requires more in-depth research.

Topics: Animals; Epinephrine; Fluid Therapy; Humans; Hypothermia, Induced; Hypovolemia; Ischemic Preconditioning; Mesenchymal Stem Cell Transplantation; Resuscitation; Shock, Hemorrhagic; Treatment Outcome; Vasopressins

Kidney dysfunction is a common complication of patients with advanced cirrhosis and is associated with poor prognosis. Patients with advanced cirrhosis show circulatory dysfunction characterized by reduced systemic vascular resistance due to splanchnic arterial vasodilation, which is caused by portal hypertension. The progressive reduction in systemic vascular resistance leads to effective arterial hypovolemia. In order to maintain arterial pressure within normal limits in this setting, there is activation of systemic vasoconstrictor systems, including the renin-angiotensin-aldosterone system, sympathetic nervous system and, in late stages, nonosmotic hypersecretion of vasopressin. Although these systems have positive effects in maintaining arterial pressure, they have a negative influence on kidney function, leading to the retention of sodium and solute-free water, and in late stages of the disease an intense kidney vasoconstriction develops, leading to decrease of the glomerular filtration rate and the development of hepatorenal syndrome (HRS). Moreover, bacterial translocation and the existence of a systemic inflammatory state in patients with advanced cirrhosis may play a role in the impairment of circulatory function. HRS is a unique cause of kidney failure of functional origin that develops in patients with cirrhosis. However, besides HRS, patients with cirrhosis may develop kidney failure due to other causes, including bacterial infections, prerenal kidney failure, shock, use of nephrotoxic drugs or intrinsic kidney diseases. Considering the existence of circulatory dysfunction and some degree of kidney vasoconstriction, patients with advanced cirrhosis have fragile kidney function and are susceptible to easily developing kidney failure associated with other complications of the disease, particularly bacterial infections and gastrointestinal bleeding.

Topics: Hemodynamics; Hepatorenal Syndrome; Humans; Hypertension, Portal; Hypovolemia; Inflammation; Kidney; Liver; Liver Circulation; Liver Cirrhosis; Vascular Resistance; Vasopressins

Critically ill patients often report distressful episodes of severe thirst, but the complex biochemical, neurohormonal mechanisms that regulate this primal sensation still elude clinicians. The most potent stimuli for thirst are subtle increases in plasma osmolality. These minute changes in osmolality stimulate central osmoreceptors to release vasopressin (also known as antidiuretic hormone). Vasopressin in turn acts on the kidneys to promote the reabsorption of water to correct the increased osmolality. If this compensatory mechanism fails to decrease osmolality, then thirst is triggered to motivate drinking. In contrast, thirst induced by marked volume loss, or hypovolemic thirst, is subject to the tight osmoregulation of the renin-angiotensin aldosterone system and accompanying adrenergic agonists. Understanding the essential role that thirst plays in salt and water regulation can provide clinicians with a better appreciation for the complex physiology that underlies this intense sensation.

Topics: Adrenergic Agonists; Critical Illness; Dehydration; Humans; Hypovolemia; Osmolar Concentration; Perception; Renin-Angiotensin System; Thirst; Vasopressins

Burn injury represents a significant problem worldwide. Advances in therapy strategies, based on better understanding of the pathophysiologic responses after burn injury have improved the clinical outcome of patients with burn injuries over the past years. This article describes the present understanding of the pathophysiology of a burn injury including both the local and systemic responses, focusing on the many facets of organ and systemic effects directly resulting from hypovolemia and circulating mediators following burn trauma.

Topics: Angiotensin II; Animals; Burns; Catecholamines; Edema; Hemodynamics; Histamine; Humans; Hypovolemia; Inflammation Mediators; Platelet Activating Factor; Prostaglandins; Serotonin; Skin; Soft Tissue Injuries; Thromboxanes; Vascular Resistance; Vasopressins

Causes of hyponatremia in children include the syndrome of appropriate antidiuretic hormone secretion, the syndrome of inappropriate antidiuretic hormone secretion and cerebral salt wasting. The purpose of this review is to distinguish these possibilities, focusing on cerebral salt wasting.. Most cases of hyponatremia in children are due to the syndrome of appropriate antidiuretic hormone secretion. The syndrome of inappropriate antidiuretic hormone secretion can be seen with neurological injury, pain and medication use. Recent studies suggest that cerebral salt wasting is a rare cause of hyponatremia. When cerebral salt wasting is diagnosed, it is often difficult to make a direct link with the central nervous system insult.. The clinical condition, assessment of extracellular fluid space volume status, measurement of urinary electrolytes and responses to infusion of saline solutions can distinguish between syndrome of appropriate antidiuretic hormone secretion, syndrome of inappropriate antidiuretic hormone secretion and cerebral salt wasting. The word 'cerebral' in 'cerebral salt wasting syndrome' can thus be inappropriate, conveying inaccurate causation.

Topics: Brain Injuries; Child; Diagnosis, Differential; Humans; Hyponatremia; Hypovolemia; Inappropriate ADH Syndrome; Sodium; Vasopressins

Bleeding of oesophageal varices and hepatorenal syndrome are most dramatic complications in gastroenterology. They develop in consequence of progressively increasing blood flow entering the vasodilated splanchnic bed and the portal vein where blood flow meets intrahepatic resistance. Porto-systemic collateral veins are formed to bypass the cirrhotic liver. Intravascular pressure is very high in these collaterals, causing the venous walls to expand into esophageal varices, which eventually may rupture and bleed. This splanchnic blood pooling generates hypovolemia in the central and arterial system, initiating activation of the renin-angiotensin-aldosteron and sympathetic nervous system. These compensatory mechanisms induce renal vasoconstriction, followed by hypoperfusion of the kidneys and development of hepatorenal syndrome. Vasoconstrictors like terlipressin inhibit splanchnic blood flow, thus reducing portal and variceal pressure, which is followed by termination ofvariceal bleeding, by normalization of central and arterial blood volume and by an improvement of kidney function and hepatorenal syndrome.

Topics: Animals; Blood Circulation; Gastrointestinal Hemorrhage; Hepatorenal Syndrome; Humans; Hypovolemia; Liver Cirrhosis; Lypressin; Splanchnic Circulation; Terlipressin; Vasoconstrictor Agents; Vasopressins

While electrolyte measurements after death may be confounded by a number of variables, vitreous humor sodium tends to remain stable for some time, enabling correlation between ante- and postmortem levels. Review of natural and unnatural causes of reduced vitreous humor sodium levels at autopsy was undertaken to demonstrate the range of diseases that may result in this finding. Natural diseases affecting the vasopressin-renin-angiotensin axis may cause reduction in sodium levels with associated hypovolemia, euvolemia, and hypervolemia. Low sodium measurements may also occur with redistribution of water, and artefactually when there are underlying lipid and protein disorders. Unnatural causes of hyponatremia at autopsy include water intoxication from psychogenic polydipsia, environmental polydipsia, ingestion of dilute infant formulas, beer potomania, endurance exercise, fresh water immersion (including water births) and iatrogenic causes including drug and parenteral fluid administration, and surgical irrigation. A knowledge of the range of conditions that may result in lowered postmortem sodium levels will help to exclude or confirm certain diseases at autopsy. In addition, significant vitreous hyponatremia may be a useful finding to help clarify mechanisms of unnatural deaths.

Topics: Drinking Behavior; Exercise; Humans; Hyponatremia; Hypovolemia; Iatrogenic Disease; Immersion; Infant Formula; Physical Endurance; Renin-Angiotensin System; Vasopressins

Osmotic and hemodynamic stress are the two primary regulators of vasopressin (VP) release from the posterior pituitary. The pathways providing information about plasma osmolality and blood pressure or blood volume are distinct and utilize different chemical neurotransmitters. Osmotic regulation of VP release is dependent upon afferents from the lamina terminalis region. Glutamate is an important transmitter in this system and angiotensinergic afferents from this region to the VP neurons modulate responses to osmotic challenges. Hemodynamic information is transmitted to the VP neurons via multisynaptic pathways from the brainstem with the A1 catecholamine neurons of the ventrolateral medulla providing the final link for information about decreases in blood pressure and volume. Several neurotransmitters and neuropeptides are expressed in the A1 neurons including norepinephrine (NE), ATP, neuropeptide Y, and substance P. The impact of co-release of these agents on VP release is reviewed and the potential physiological significance is discussed.

Topics: Animals; Blood; Humans; Hypotension; Hypovolemia; Neurotransmitter Agents; Vasopressins; Water-Electrolyte Balance

Topics: Animals; Cerebral Ventricles; Cholecystokinin; Female; Hypothalamus; Hypovolemia; Lactation; Median Eminence; Neurons; Neurosecretory Systems; Oxytocin; Pregnancy; Subfornical Organ; Vasopressins; Water-Electrolyte Balance

We conducted an open, randomized, and prospective study to determine the effect of hypertonic saline on the secretion of antidiuretic hormone (ADH) and aldosterone in children with severe head injury (Glasgow coma scale <8). Thirty-one consecutive patients at a level III pediatric intensive care unit at a children's hospital received either lactated Ringer's solution (Ringer's group, n = 16) or hypertonic saline (Hypertonic Saline group, n = 15) over a 3-day period. Serum ADH levels were significantly larger in the Hypertonic Saline group as compared with the Ringer's group (P = 0.001; analysis of variance) and were correlated to sodium intake (Ringer's group: r = 0.39, R(2) = 0.15, P = 0.02; Hypertonic Saline group: r = 0.42, R(2) = 0.18, P = 0.02) and volume of fluids given IV (Ringer's group: r = 0.38, R(2) = 0.15, P = 0.02; Hypertonic Saline group: r = 0.32, R(2) = 0.1, P = not significant). Correlation of ADH to plasma osmolality was significant if plasma osmolality was >280 mOsm/kg (r = 0.5, R(2) = 0.25, P = 0.06), indicating an osmotic threshold for ADH release. Serum aldosterone levels were larger on the first day than during Days 2 and 3 in both groups and inversely correlated to serum sodium levels only in the Ringer's group (r = -0.55, R(2) = 0.3, P < 0.001). This group received a significantly larger fluid volume on Day 1 (P = 0.05, Mann-Whitney U-test) than did patients in the Hypertonic Saline group, indicating hypovolemia during the first day. Head-injured children have appropriate levels of ADH. They may be hypovolemic during the first day of treatment, especially if they receive lactated Ringer's solution.. In head-injured patients, we recommend fluid restriction to avoid inappropriate secretion of antidiuretic hormone. In a prospective, randomized, and controlled study in 31 children, we were able to show that the antidiuretic hormone levels are appropriate in response to hypovolemia, sodium load, or both.

Topics: Adolescent; Aldosterone; Child; Child, Preschool; Craniocerebral Trauma; Humans; Hypovolemia; Infant; Isotonic Solutions; Prospective Studies; Ringer's Lactate; Saline Solution, Hypertonic; Sodium; Vasopressins

An attenuated baroreflex response and orthostatic intolerance have been reported in endurance-trained male athletes; however, it is still unknown whether this occurs also in females. The purpose of the present study was to examine whether endurance exercise-trained women had a predisposition to orthostatic compromise, and if so, what causative factor(s) may induce orthostatic intolerance.. We studied cardiovascular and hormonal responses to graded lower body negative pressure (LBNP) (0 to -60 mm Hg) in 26 middle-distance female runners (18.6 +/- 0.1 yr) as the exercise-trained (ET) subjects and 23 age-matched untrained (UT) control subjects. On the basis of the occurrence of syncope episodes during LBNP, ET and UT subjects were further allocated to two groups; ET with presyncope (ET+syncope) and without presyncope (ET-syncope) and UT with presyncope (UT+syncope) and without presyncope (UT-syncope).. Occurrence of presyncope episodes during LBNP was higher in ET (65.4%, P < 0.05) than that for UT (34.8%). Leg compliance was higher (P < 0.05) in ET than in UT. LBNP reduced stroke volume (SV) more (P < 0.05), increased heart rate (HR) higher (P < 0.05), and increased forearm vascular resistance (FVR) more in ET+syncope as compared with the other groups. Response of vasoactive hormones to LBNP was higher in ET+syncope (P < 0.05) than that of the other groups except for norepinephrine (NE); high in both ET+syncope and UT+syncope. The relationship between SV and NE, an index of sympathetic neuronal response, had no training-related changes during LBNP.. We conclude that exercise-trained females have a high incidence of orthostatic intolerance during LBNP, with a greater reduction of SV independent of changes in baroreflex and neurohumoral function. A lower incidence of LBNP intolerance in UT may be accounted for by a lower reduction of SV during LBNP. An increase in leg compliance in the exercise-trained females may play an important role in inducing pronounced reduction of SV and hence the intolerance to LBNP.

Topics: Adolescent; Adult; Baroreflex; Female; Humans; Hypotension, Orthostatic; Hypovolemia; Lower Body Negative Pressure; Norepinephrine; Physical Endurance; Renin; Running; Sex Factors; Stroke Volume; Syncope; Vasopressins

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

Vasovagal reflex is the most common type of syncope but its etiology is not fully elucidated. Venous return and cardiac output are key in hemodynamic control. The aim of the study was to assess cardiovascular biomarkers and echocardiographic measures at rest and during hypovolemia in women with and without a history of vasovagal syncope.. Fourteen women (aged 18-30) suffering from recurrent vasovagal syncope and 15 age-matched healthy women were included. Graded lower body negative pressure (LBNP) was used to create central hypovolemic stress until signs of presyncope occurred. Echocardiography was applied at rest and throughout LBNP. Cardiovascular biomarkers: copeptin, mid-regional proadrenomedullin, mid-regional pro-ANP, C-terminal proendothelin-1, and plasma norepinephrine were measured both at rest and throughout graded hypovolemia to presyncope.. Women prone to vasovagal syncope demonstrate reduced cardiac preload, lower cardiac output, as well as increased release of vasopressin in rest and during hypovolemic challenge. The results emphasize the importance of venous return and cardiac output in the pathogenesis of vasovagal syncope.

Topics: Adolescent; Adult; Biomarkers; Cardiac Output; Case-Control Studies; Echocardiography, Three-Dimensional; Endothelin-1; Female; Glycopeptides; Hemodynamics; Humans; Hypovolemia; Lower Body Negative Pressure; Norepinephrine; Peptide Fragments; Predictive Value of Tests; Recurrence; Sex Factors; Stress, Physiological; Syncope, Vasovagal; Time Factors; Vasopressins; Young Adult

Central hypovolemia induced by orthostatic loading causes reno-vascular changes that can lead to orthostatic intolerance. In this study, we investigated volume regulating hormonal responses and reno-vascular changes in male and female subjects as they underwent central hypovolemia, induced by graded lower body negative pressure (LBNP). Aquaporin-2 (AQP2) excretion was measured as a biomarker for the renal system response to vasopressin. 37 young healthy subjects (n = 19 males; n = 18 females) were subjected to graded LBNP until - 40 mmHg LBNP. Under resting conditions, males had significantly higher copeptin (a stable peptide derived from vasopressin) levels compared with females. Adrenocorticotropin (ACTH), adrenomedullin (ADM), vasopressin (AVP) and brain natriuretic peptide (BNP) were not affected by our experimental protocol. Nevertheless, an analysis of ADM and BNP with the data normalized as percentages of the baseline value data showed an increase from baseline to 10 min after recovery in the males in ADM and in the females in BNP. Analysis of BNP and ADM raises the possibility of a preferential adaptive vascular response to central hypovolemia in males as shown by the normalized increase in ADM, whereas females showed a preferential renal response as shown by the normalized increase in BNP. Furthermore, our results suggest that there might be a difference between men and women in the copeptin response to alterations in orthostatic loading, simulated either using LBNP or during posture changes.

Topics: Adult; Aquaporin 2; Blood Pressure; Cardiac Output; Female; Heart Rate; Humans; Hypovolemia; Lower Body Negative Pressure; Male; Neurophysins; Protein Precursors; Sex Factors; Vascular Resistance; Vasopressins; Young Adult

This study compared the effects of vasopressin via tibial intraosseous (IO) and intravenous (IV) routes on maximum plasma concentration (Cmax), the time to maximum concentration (Tmax), return of spontaneous circulation (ROSC), and time to ROSC in a hypovolemic cardiac arrest model.. This study was a randomized prospective, between-subjects experimental design. A computer program randomly assigned 28 Yorkshire swine to one of four groups: IV (n=7), IO tibia (n=7), cardiopulmonary resuscitation (CPR) + defibrillation (n=7), and a control group that received just CPR (n=7). Ventricular fibrillation was induced, and subjects remained in arrest for two minutes. CPR was initiated and 40 units of vasopressin were administered via IO or IV routes. Blood samples were collected at 0.5, 1, 1.5, 2, 2.5, 3, and 4 minutes. CPR and defibrillation were initiated for 20 minutes or until ROSC was achieved. We measured vasopressin concentrations using high-performance liquid chromatography.. There was no significant difference between the IO and IV groups relative to achieving ROSC (p=1.0) but a significant difference between the IV compared to the CPR+ defibrillation group (p=0.031) and IV compared to the CPR-only group (p=0.001). There was a significant difference between the IO group compared to the CPR+ defibrillation group (p=0.031) and IO compared to the CPR-only group (p=0.001). There was no significant difference between the CPR + defibrillation group and the CPR group (p=0.127). There was no significant difference in Cmax between the IO and IV groups (p=0.079). The mean ± standard deviation of Cmax of the IO group was 58,709±25, 463 pg/mL compared to the IV group, which was 106,198±62, 135 pg/mL. There was no significant difference in mean Tmax between the groups (p=0.084). There were no significant differences in odds of ROSC between the tibial IO and IV groups.. Prompt access to the vascular system using the IO route can circumvent the interruption in treatment observed with attempting conventional IV access. The IO route is an effective modality for the treatment of hypovolemic cardiac arrest and may be considered first line for rapid vascular access.

Topics: Animals; Cardiopulmonary Resuscitation; Disease Models, Animal; Electric Countershock; Heart Arrest; Hypovolemia; Infusions, Intraosseous; Infusions, Intravenous; Male; Random Allocation; Swine; Vasoconstrictor Agents; Vasopressins

The American Heart Association (AHA) recommends intravenous (IV) or intraosseous (IO) vasopressin in Advanced Cardiac Life Support (ACLS). Obtaining IV access in hypovolemic cardiac arrest patients can be difficult, and IO access is often obtained in these life threatening situations. No studies have been conducted to determine the effects of humeral IO (HIO) access with vasopressin in the return of spontaneous circulation (ROSC). Our study compared the kinetics of vasopressin and ROSC with HIO with IV access in the hypovolemic swine model.. Twenty-two Yorkshire swine were divided into three groups: HIO (n = 7), IV (n = 8), and a control group (n = 7). The IV and HIO group received vasopressin and cardiopulmonary resuscitation (CPR), while the control group received only CPR. All subjects were exsanguinated 31 percent of their blood volume, placed in cardiac arrest, and resuscitated per ACLS. Subjects that achieved ROSC were then monitored for 20 minutes. Blood samples (10 mL) collected at 0.5, 1, 1.5, 2, 2.5, 3, and 4 minutes after vasopressin injection and analyzed for maximum concentration (Cmax) and time to maximum concentration (Tmax). Data were analyzed using a multivariate analysis of variance (MANOVA) and a Fisher's Exact Test.. ROSC was achieved in every subject that received vasopressin via the HIO route. Data analysis using a MANOVA pairwise comparison revealed no difference between mean Cmax (p = 0.601) and Tmax (p = 0.771) of vasopressin administered IV versus HIO routes. Analysis of the mean serum concentrations at time intervals using a repeated measures analysis of variance found no difference (p > 0.05). A Fisher's Exact Test revealed no difference in rate of ROSC between HIO and IV groups (p > 0.05). Odds ratio determined that there was a 33 times higher chance of survival among HIO subjects versus control (CPR and Defibrillation; p = 0.03) and no difference in the survivability of the HIO or IV groups (p = 0.52).. The data from this study strongly suggest that there is no significant difference in ROSC, time to ROSC, hemodynamics, or pharmacokinetics between HIO vasopressin and IV vasopressin. This research reinforces current AHA guidelines recommending the use of HIO route early over delaying care awaiting IV access.

Topics: Animals; Cardiopulmonary Resuscitation; Disease Models, Animal; Heart Arrest; Hypovolemia; Infusions, Intraosseous; Infusions, Intravenous; Male; Random Allocation; Swine; Vasoconstrictor Agents; Vasopressins

Hyponatremia is a serious, but often overlooked, electrolyte imbalance that has been independently associated with a wide range of deleterious changes involving many different body systems. Untreated acute hyponatremia can cause substantial morbidity and mortality as a result of osmotically induced cerebral edema, and excessively rapid correction of chronic hyponatremia can cause severe neurologic impairment and death as a result of osmotic demyelination. The diverse etiologies and comorbidities associated with hyponatremia pose substantial challenges in managing this disorder. In 2007, a panel of experts in hyponatremia convened to develop the Hyponatremia Treatment Guidelines 2007: Expert Panel Recommendations that defined strategies for clinicians caring for patients with hyponatremia. In the 6 years since the publication of that document, the field has seen several notable developments, including new evidence on morbidities and complications associated with hyponatremia, the importance of treating mild to moderate hyponatremia, and the efficacy and safety of vasopressin receptor antagonist therapy for hyponatremic patients. Therefore, additional guidance was deemed necessary and a panel of hyponatremia experts (which included all of the original panel members) was convened to update the previous recommendations for optimal current management of this disorder. The updated expert panel recommendations in this document represent recommended approaches for multiple etiologies of hyponatremia that are based on both consensus opinions of experts in hyponatremia and the most recent published data in this field.

Topics: Adrenal Insufficiency; Antidiuretic Hormone Receptor Antagonists; Clinical Trials as Topic; Diagnosis, Differential; Diuretics; Gastrointestinal Diseases; Genetic Diseases, X-Linked; Humans; Hyponatremia; Hypothyroidism; Hypovolemia; Inappropriate ADH Syndrome; Liver Cirrhosis; Polydipsia; Receptors, Vasopressin; Sodium Chloride; Vasopressins

This study evaluated the osmoregulatory system changes in 39 patients with severe ovarian hyperstimulation syndrome. Plasma osmolality (Posm) less or more than 280 mOsm/kg body weight were associated with inappropriate antidiuretic hormone secretion syndrome and hypovolemia, respectively.

Topics: Adult; Dinoprostone; Female; Humans; Hypovolemia; Inappropriate ADH Syndrome; Osmolar Concentration; Ovarian Hyperstimulation Syndrome; Ovulation Induction; Severity of Illness Index; Vasopressins; Water-Electrolyte Balance; Young Adult

This study was performed to investigate the effects of L-thyroxine treatment on plasma vasopressin (AVP) levels in rats with hypothyroidism induced by propylthiouracil (PTU). Animals were separated into three groups each having 6 rats: control, PTU, PTU+L-thyroxine groups. Then, the groups were further divided into 3 sub-groups including 6 rats (a; basal, b; hypertonic stimulated and c; hypovolemic stimulated). At the end of the experiments all rats were decapitated in order to obtain plasma samples for analysis in terms of Hct, osmolality, TT 3 , TT 4 and vasopressin. Haematocrit (Hct) levels were the highest in hypovolemic stimulated sub-group (P < 0.001). Osmolality levels were higher in hypertonic stimulated sub-groups (P < 0.001). Total T 3 and T 4 values were the lowest in the PTU group and the highest in the L-thyroxine treated group (P < 0.001). Plasma AVP levels were reduced by hypothyroidism. However, L-thyroxine treatment after the hypothyroidism prevented this reduction (P < 0.001). Vasopressin responses to basal, hypovolemic and hypertonic stimulations were the lowest in the PTU group (P < 0.001). The results of the present study show that basal and stimulated plasma vasopressin levels are reduced in PTU-induced hypothyroidism. However, L-thyroxine treatment following hypothyroidism prevents this reduction.

Topics: Animals; Antithyroid Agents; Body Weight; Dietary Supplements; Hypertonic Solutions; Hypothyroidism; Hypovolemia; Male; Propylthiouracil; Rats; Rats, Wistar; Thyroxine; Vasopressins

Although hyponatremia occurs in most patients with severe malaria, its pathogenesis, prognostic significance, and optimal management have not been established. Clinical and biochemical data were prospectively collected from 171 consecutive Bangladeshi adults with severe malaria. On admission, 57% of patients were hyponatremic. Plasma sodium and Glasgow Coma Score were inversely related (r(s) = -0.36, P < 0.0001). Plasma antidiuretic hormone concentrations were similar in hyponatremic and normonatremic patients (median, range: 6.1, 2.3-85.3 versus 32.7, 3.0-56.4 pmol/L; P = 0.19). Mortality was lower in hyponatremic than normonatremic patients (31.6% versus 51.4%; odds ratio [95% confidence interval]: 0.44 [0.23-0.82]; P = 0.01 by univariate analysis). Plasma sodium normalized with crystalloid rehydration from (median, range) 127 (123-140) mmol/L on admission to 136 (128-149) mmol/L at 24 hours (P = 0.01). Hyponatremia in adults with severe malaria is common and associated with preserved consciousness and decreased mortality. It likely reflects continued oral hypotonic fluid intake in the setting of hypovolemia and requires no therapy beyond rehydration.

Topics: Acetylcysteine; Adolescent; Adult; Aged; Bangladesh; Female; Glasgow Coma Scale; Humans; Hyponatremia; Hypovolemia; Malaria; Male; Middle Aged; Seasons; Sodium; Vasopressins; Young Adult

The present study was conducted to determine the effects of basal, isotonic as well as hypertonic and hypovolemic treatments on fluid-electrolyte balance and plasma AVP levels in rats supplemented with L-thyroxine and pinealectomized L-thyroxine. The animals were initially separated into 4 groups: control (n = 24), L-thyroxine treated (n = 24); L-thyroxine + sham-pinealectomy (n = 24) treated and 4-L-thyroxine + pinealectomy (n = 24) treated. L-thyroxine was given for 4 weeks. At the end of the 4-week experimental period, the sub-groups were formed before decapitation, which were classified as unstimulated (n = 6), isotonic (n = 6), hypertonic (n = 6) and hypovolemic (n = 6) stimulation. Plasma AVP, total triiodothyronine (TT3) and total thyroxine (TT4) levels were examined in plasma by RIA. Hematocrit and osmolality levels were also determined. It was found that the TT3 and TT4 levels showed significant increases in L-thyroxine treated groups (P <0.001). Also, plasma AVP levels increased in the group subjected to L-thyroxine treatment. However, this increase was depicted to be significantly more prominent in L-thyroxine + pinealectomy treated group (P <0.001). The results of the present study indicate that L-thyroxine treatment increases the basal and stimulated AVP release, which became more significant in the pinealectomy plus L-thyroxine treatment group. Moreover, the results indicate that AVP response to hypertonic and hypovolemic stimulations does not undergo any change due to supplementation by L-thyroxine treatment and/or pinealectomy plus L-thyroxine.

Topics: Animals; Hematocrit; Hypertonic Solutions; Hypotonic Solutions; Hypovolemia; Male; Melatonin; Pineal Gland; Rats; Rats, Sprague-Dawley; Sodium Chloride; Thyroxine; Vasopressins

Neuronal activity regulated pentraxin (Narp) is a secreted, synaptic protein that has been implicated in modulating synaptic transmission. However, it is unclear how Narp secretion is regulated. Since we noted prominent Narp immunostaining in vasopressin neurons of the hypothalamus and in the posterior pituitary, we assessed whether it, like vasopressin, is released into the systemic circulation in an activity-dependent fashion. Consistent with this hypothesis, electron microscopic studies of the posterior pituitary demonstrated that Narp is located in secretory vesicles containing vasopressin. Using affinity chromatography, we detected Narp in plasma and found that these levels are markedly decreased by hypophysectomy. In addition, we confirmed that injection of a viral Narp construct into the hypothalamus restores plasma Narp levels in Narp knockout mice. In checking for activity-dependent secretion of Narp from the posterior pituitary, we found that several stimuli known to trigger vasopressin release, i.e. hypovolemia, dehydration and endotoxin, elevate plasma Narp levels. Taken together, these findings provide compelling evidence that Narp is secreted from vasopressin neurons in an activity-dependent fashion.

Topics: Adenoviridae; Animals; C-Reactive Protein; Chromatography, Affinity; Dehydration; DNA, Complementary; Genetic Vectors; Humans; Hypovolemia; Immunohistochemistry; Lipopolysaccharides; Mice; Mice, Knockout; Microscopy, Electron; Microscopy, Immunoelectron; Motor Activity; Nerve Tissue Proteins; Neurons; Pituitary Gland; Rats; Rats, Sprague-Dawley; Restraint, Physical; Stress, Psychological; Vasopressins

Neonatal foals succumb rapidly to hypovolaemic shock in comparison to mature horses; they do not consistently increase their heart rate in response to hypotension and respond differently to fluid administration. The hormonal responses to hypovolaemia in the horse and foal require investigation.. The hormonal responses to hypovolaemia and fluid administration differ between mature and neonatal horses.. Five mature horses and 5 neonatal foals fulfilling predetermined criteria for hypovolaemia, were included in the study. A blood sample was taken at admission and after normalisation of fluid balance. These were analysed for plasma aldosterone, vasopressin (AVP) and atrial natriuretic peptide (ANP). Normally distributed variables were compared using the Student's t test and nonparametric data using the Mann-Whitney U test.. ANP, AVP and aldosterone were higher before fluid resuscitation than after fluid resuscitation in mature horses. Aldosterone was higher before than after fluid resuscitation in foals, and was higher in foals both before and after fluid resuscitation than in mature horses. ANP was lower in mature horses after fluid resuscitation than in foals. No other comparisons were significantly different.. The hormonal responses of the mature and neonatal horses are different during hypovolaemia and following fluid resuscitation.. The differences in the hormonal responses to hypovolaemia and fluid resuscitation may be important when considering fluid resuscitation of hypovolaemic horses and foals, and warrants further investigation.

Topics: Aging; Aldosterone; Animals; Animals, Newborn; Atrial Natriuretic Factor; Body Fluids; Female; Fluid Therapy; Horse Diseases; Horses; Hypovolemia; Male; Statistics, Nonparametric; Treatment Outcome; Vasopressins

The present studies investigated the influence of presystemic signals on the control of thirst, salt appetite, and vasopressin (VP) secretion in rats during nonhypotensive hypovolemia. Rats were injected with 30% polyethylene glycol (PEG) solution, deprived of food and water overnight, and then allowed to drink water, 0.15 M NaCl, or 0.30 M NaCl. The PEG treatment, which produced 30-40% plasma volume deficits, elicited rapid intakes in an initial bout of drinking, but rats consumed much more 0.15 M NaCl than water or 0.30 M NaCl. In considering why drinking stopped sooner when water or concentrated saline was ingested, it seemed relevant that little or no change in systemic plasma Na(+) concentration was observed during the initial bouts and that the partial repair of hypovolemia was comparable, regardless of which fluid was consumed. In rats that drank 0.15 M NaCl, gastric emptying was fastest and the combined volume of ingested fluid in the stomach and small intestine was largest. These and other observations are consistent with the hypothesis that fluid ingestion by hypovolemic rats is inhibited by distension of the stomach and proximal small intestine and that movement of dilute or concentrated fluid into the small intestine provides another presystemic signal that inhibits thirst or salt appetite, respectively. On the other hand, an early effect of water or saline consumption on VP secretion in PEG-treated rats was not observed, in contrast to recent findings in dehydrated rats. Thus the controls of fluid ingestion and VP secretion are similar but not identical during hypovolemia.

Topics: Animals; Appetite; Blood Proteins; Drinking Behavior; Gastric Emptying; Hypovolemia; Male; Polyethylene Glycols; Rats; Rats, Sprague-Dawley; Sodium Chloride; Thirst; Time Factors; Vasopressins

Symptoms of hyponatremia and diuresis due to cerebral salt wasting syndrome (CSWS) are often observed after aneurysmal subarachnoid hemorrhage (SAH). Inadequately treated CSWS is known to work as a trigger of symptomatic vasospasm in SAH patients. Therefore, it is indispensable to detect and treat CSWS as early as possible in ICU. A 36-year-old man with SAH was admitted to our ICU. His urine volume increased excessively 3 days after ICU admission, and it reached a peak (39,250 ml x day(-1)) on the 6th day in ICU. Since infusion volume was controlled with regard to daily urinary output, hyponatremia was not noticeable and excessive urine volume stood out conspicuously. Though vasopressin and desmopressin were administered, the symptoms of natriuresis and hyponatremia were aggravated, associated with hyper secretion of natriuretic peptides (ANP 160 pg x dl(-1), BNP 172 pg x dl(-1)). Recent studies revealed that hyponatremia and hypovolemia following SAH might be caused by exaggerated secretion of natriuretic peptides. Experimental studies showed that the administration of vasopressin and desmopressin cause excessive secretion of natriuretic peptides under the circumstance of volume expansion in rats. We infer that the administration of vasopressin and desmopressin to our patient deterionated natriuresis in CSWS as in the previous experimental findings.

Topics: Adult; Animals; Atrial Natriuretic Factor; Brain Diseases; Contraindications; Humans; Hyponatremia; Hypovolemia; Male; Natriuresis; Rats; Subarachnoid Hemorrhage; Syndrome; Urination Disorders; 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

The present study was performed to determine how l-thyroxine-induced hyperthyroidism affects the vasopressin response to different stimulations (isotonic, hypertonic and hypovolemic) in rats. Spraque-Dawley rats were initially separated into 3 groups; control (n=24), sham hyperthyroidism (n=24, hyperthyroidism (n=24). At the end of the experiment additional sub-groups were formed before decapitation. These sub-groups were formed as; without stimulation (n=6), isotonic stimulation (n=6), hypertonic stimulation (n=6) and hypovolemic stimulation (n=6). Total T3, total T4 and AVP levels were evaluated in the plasma. Haematocrit and osmolality levels were also determined. When the parameters related to thyroid hormones were evaluated, it was determined that total T3 and T4 levels were higher in hyperthyroid group than the other groups. Plasma AVP levels showed more increase in hyperthyroid group both in basal grade and against to hypertonic and hypovolemic stimulations than the other groups (P<0.001). The results of the present study indicate that l-thyroxine-induced experimental hyperthyroidism increased basal and stimulated AVP release in rats.

Topics: Animals; Body Weight; Hematocrit; Hyperthyroidism; Hypertonic Solutions; Hypovolemia; Isotonic Solutions; Male; Osmolar Concentration; Rats; Rats, Sprague-Dawley; Thyroxine; Triiodothyronine; Vasopressins; Water-Electrolyte Balance

The mortality induced by severe sepsis and septic shock remains very elevated despite progress in diagnosis and treatment. All the experts in the field consider that further progress is possible with better and more prompt use of the treatments now available. The "Surviving Sepsis" campaign reviews the diverse treatments that can be used and the best ways to prescribe them. It also proposes two bundles of objectives to be completed systematically for all patients: the first within the first 6 hours, the second between the sixth and 24th hour. Encouraging results show that applying these therapeutic principles can reduce mortality by 30% (relative percentage) compared with a treatment without specific objectives.

Topics: Anti-Bacterial Agents; Anti-Inflammatory Agents; Humans; Hydrotherapy; Hypovolemia; Practice Guidelines as Topic; Sepsis; Shock, Septic; Survivors; Vasopressins

Accumulated evidence indicates attenuated vasopressin (AVP) release associated with hyperbaria in humans. The present study was designed to test the hypothesis that plasma AVP response to central hypovolemia was attenuated in a hyperbaric environment.. Response of AVP to central hypovolemic stress, in the form of lower-body negative pressure (LBNP), was measured in 10 men at 1 and 3 atmosphere absolute (ATA) air. The stress consisted of 4 min each of control and LBNP at -20 and -40 mmHg. Plasma AVP, plasma norepinephrine (NE), plasma osmolality, and hematocrit (Hct) were measured. Thoracic impedance (Z0), and leg volume were also determined.. The baseline AVP (0.9 +/- 0.3 pg x ml(-1)) at 1 ATA increased significantly in response to -40 mmHg LBNP (1.8 +/- 0.6 pg x ml(-1)), but the increase was attenuated at 3 ATA (1.2 +/- 0.8 pg x ml(-1)). The baseline NE at 3 ATA was lower by 22.4 pg x ml(-1) than that of 1 ATA (226.5 pg x ml(-1)). NE increased with increasing LBNP at both environmental pressures, but the increase was independent of the pressure. Changes in Z0, reflecting thoracic blood volume, were identical in both environments. Mean arterial pressure, plasma osmolality, and Hct remained constant throughout the experimental period. Leg volume increased stress dependently during LBNP (approximately 34 ml at -20 mmHg; approximately 74 ml at -40 mmHg) and the increment was similar in the two environments.. The present study revealed that hyperbaria attenuated the response of AVP and NE to hypovolemic stress. The attenuated AVP response to LBNP was associated with neither plasma osmolality nor intrathoracic blood shift.

Topics: Adult; Atmospheric Pressure; Hematocrit; Humans; Hypovolemia; Male; Norepinephrine; Pressoreceptors; Regional Blood Flow; Thorax; Vasopressins

We describe the treatment of two patients with hemorrhagic shock unresponsive to volume replacement and catecholamines. Both patients responded to a small-dose infusion of vasopressin, which allowed tapering off of the catecholamines. The possible role of small-dose infusions of vasopressin in fluid- and catecholamine-resistant hemorrhagic shock is discussed.

Topics: Blood Loss, Surgical; Blood Volume; Catecholamines; Digestive System Surgical Procedures; Gastrointestinal Neoplasms; Humans; Hypovolemia; Male; Middle Aged; Pancreaticoduodenectomy; Shock, Hemorrhagic; Stomach Neoplasms; Vasoconstrictor Agents; Vasopressins

Although acute decreases in plasma volume are known to enhance the osmotically induced arginine vasopressin (AVP) release, it is unclear whether there is also such interaction at the level of gene transcription. It also remains to be established how sustained changes in plasma volume affect the osmoregulation. In this study, we examined how acute and chronic decreases in blood volume affected the osmoregulation of AVP release and gene transcription in rats. Acute hypovolemia was induced by intraperitoneal injection of polyethylene glycol (PEG), and chronic hypovolemia was induced by 3 days of water deprivation (WD) or 12 days of salt loading (SL). Rats were injected with isotonic or hypertonic saline, and plasma AVP levels and AVP heteronuclear (hn)RNA expression in the supraoptic and paraventricular nuclei, an indicator of gene transcription, were examined in relation to plasma osmolality in each group. Plasma AVP levels were correlated with plasma Na levels in all groups. Whereas the regression lines relating plasma AVP to Na were almost identical among control, WD, and SL groups, the thresholds of plasma Na for AVP release were significantly decreased only in the PEG group. AVP hnRNA levels were also correlated with plasma Na levels in control and PEG groups, and the thresholds were significantly decreased in the PEG group. In contrast, there was no significant correlation of AVP hnRNA and plasma Na levels in WD and SL groups. Thus it was demonstrated that acute and chronic reduction in plasma volume affected the osmoregulation of AVP release and gene transcription in different ways.

Topics: Acute Disease; Animals; Blood Proteins; Chronic Disease; Gene Expression Regulation; Hypovolemia; Male; Plasma Volume; Polyethylene Glycols; Rats; Rats, Sprague-Dawley; Sodium; Transcription, Genetic; Vasopressins; Water-Electrolyte Balance

The set points for vasopressin release in response to increasing plasma osmolality and hypovolaemia alter with reproductive status. Here, we studied stimulated vasopressin release following ovariectomy and oestrogen replacement, neuronal activity being measured in terms of immediate early gene expression. Observations were carried out on three groups of female Sprague-Dawley rats. The first group were ovariectomized. The second group were given a subcutaneous oestrogen implant (20 microg/ml oestradiol-17 beta) at the time of ovariectomy. The final group were left intact and observations performed at oestrus. Two weeks after ovariectomy, vascular cannulae were implanted under anaesthesia and at least 48 h allowed for recovery before hormone release was stimulated by infusion of 1.5 M NaCl for 90 min, or hypovolaemia induced by the removal of 10 mg/kg body weight taken in 1-ml aliquots. Blood pressure was monitored, and blood samples were taken for determination of packed cell volume and plasma vasopressin and osmolality. After a minimum of 48 h, the challenge was repeated, the rats anaesthetized, and perfused with 4% paraformaldehyde. Brain sections were processed for immunocytochemical detection of Fos protein. Vasopressin release in response to both stimuli was reduced in ovariectomized compared to intact rats and the response could be substantially restored by oestradiol replacement. The number of Fos positive cells in the supraoptic nucleus of oestrogen-replaced rats was significantly higher than in the ovariectomized group and not statistically different from the intact group.

Topics: Adaptation, Physiological; Analysis of Variance; Animals; Blood Volume; Estradiol; Estrous Cycle; Female; Genes, Immediate-Early; Hypovolemia; Immunohistochemistry; Osmolar Concentration; Ovariectomy; Proto-Oncogene Proteins c-fos; Rats; Rats, Sprague-Dawley; Supraoptic Nucleus; Tissue Distribution; Vasopressins; Water-Electrolyte Balance

Medullary catecholamine and hypothalamic neurosecretory oxytocin cells are activated by hypotension, but previous studies have provided uncertain outcomes concerning their ability to respond to a purely hypovolaemic stimulus. In the present study, injections of PEG/water and pentolinium were used to elicit non-hypotensive, isosmotic hypovolaemia and isovolaemic, isosmotic hypotension, respectively, in conscious rats. Animals were sacrificed 2 h after treatment. Immunolabelling for Fos, tyrosine hydroxylase and oxytocin established that these two stimuli activate almost identical populations of catecholamine neurons in the ventrolateral and dorsomedial medulla, and very similar populations of oxytocin cells in the supraoptic and paraventricular nuclei of the hypothalamus.

Topics: Animals; Antihypertensive Agents; Blood Pressure; Catecholamines; Hypotension; Hypovolemia; Medulla Oblongata; Neurons; Oxytocin; Paraventricular Hypothalamic Nucleus; Pentolinium Tartrate; Polyethylene Glycols; Proto-Oncogene Proteins c-fos; Rats; Rats, Wistar; Supraoptic Nucleus; Tyrosine 3-Monooxygenase; Vasopressins

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

In the present study we have used the detection of Fos, the protein product of c-fos, to determine the distribution of neurons in the medulla and hypothalamus that are activated by changes in central blood volume. Experiments were conducted in both barointact and barodenervated conscious rabbits, to determine the contribution of arterial baroreceptors to the pattern of Fos expression evoked by changes in central blood volume, induced either by intravenous infusion of an isotonic modified gelatin solution, or by partial occlusion of the vena cava. These procedures resulted in a significant increase and decrease, respectively, in right atrial pressure over a 60 min period. In control experiments, barointact and barodenervated rabbits were subjected to the identical procedures except that no changes in central blood volume were induced. In comparison with the control observations, central hypervolaemia produced a significant increase in the number of Fos-immunoreactive neurons in the nucleus tractus solitarius, area postrema, the caudal, intermediate and rostral parts of the ventrolateral medulla, supraoptic nucleus, paraventricular nucleus, arcuate nucleus, suprachiasmatic nucleus and median preoptic nucleus. The overall pattern of Fos expression induced by central hypervolaemia did not differ significantly between barointact and barodenervated animals. Similarly, the overall pattern of Fos expression induced by central hypovolaemia did not differ significantly between barointact and barodenervated animals, but did differ significantly from that produced by hypervolaemia. In particular, central hypovolaemia produced a significant increase in Fos expression in the same regions as above, but also in the subfornical organ and organum vasculosum lamina terminalis. In addition, compared with central hypervolaemia, hypovolaemia produced a significantly greater degree of Fos expression in the rostral ventrolateral medulla and supraoptic nucleus. Furthermore, double-labelling for tyrosine hydroxylase immunoreactivity demonstrated that neurons in the ventrolateral medulla that expressed Fos following hypovolaemia were predominantly catecholamine cells, whereas following hypervolaemia they were predominantly non-catecholamine cells. Finally, double-labelling for vasopressin immunoreactivity demonstrated that the number of Fos/vasopressin immunoreactive cells in the supraoptic nucleus was approximately 10 times greater following hypovolaemia compared with hypervolaemi

Topics: Animals; Aorta; Blood Volume; Cardiovascular Physiological Phenomena; Carotid Sinus; Consciousness; Denervation; Genes, Immediate-Early; Hypertension; Hypotension; Hypovolemia; Male; Neurons; Paraventricular Hypothalamic Nucleus; Pressoreceptors; Proto-Oncogene Proteins c-fos; Rabbits; Solitary Nucleus; Tyrosine 3-Monooxygenase; Vasopressins

We have used in situ hybridization and radio-immunoassay to compare temporal dynamics of components in the hypothalamo-pituitary limb of the hypothalamo-pituitary-adrenal axis during sustained hypovolemic stress in adrenalectomized (ADX) rats to those previously reported in intact animals. We asked three questions: first, does corticotropin-releasing hormone (CRH) gene transcription occur in neuroendocrine neurones of the hypothalamic paraventricular nucleus (PVH) of ADX rats, and if so, how is it temporally organized; second, what is the expression pattern of the vasopressin and other genes known to be colocalized in these neuroendocrine neurones; third, if adrenocorticotropin hormone (ACTH) secretion occurs, what is its temporal profile? We found that sustained hypovolemia evoked a brief episode of CRH gene transcription in ADX rats that occurred earlier than in intact rats. However, in contrast to saline-injected controls, this activation was not maintained because declines in CRH hnRNA and mRNA were seen as the stress continued. Although increased vasopressin gene transcription was not seen in intact hypovolemic rats, robust increases were measured throughout in ADX rats, suggesting that in the absence of corticosterone the vasopressin gene is transcribed preferentially to the CRH gene during sustained hypovolemia. c-fos and preproenkephalin mRNA profiles also exhibited earlier onsets compared to intact rats. Finally, the onset and duration of ACTH secretion was the same in ADX rats as previously reported in intact rats. Collectively, these data support two hypotheses regarding the actions of corticosterone. First, that it provides some form of facilitatory signal allowing neuroendocrine CRH transcriptional mechanisms to remain active during sustained hypovolemia. Second, that it strongly inhibits the response of the vasopressin gene to hypovolemic stress.

Topics: Adrenalectomy; Adrenocorticotropic Hormone; Animals; Cell Count; Corticosterone; Corticotropin-Releasing Hormone; Enkephalins; Gene Expression; Hematocrit; Hypovolemia; Injections, Subcutaneous; Male; Neuropeptides; Organ Size; Paraventricular Hypothalamic Nucleus; Polyethylene Glycols; Protein Precursors; Proto-Oncogene Proteins c-fos; Rats; Rats, Sprague-Dawley; RNA, Messenger; Stress, Physiological; Thymus Gland; 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

Topics: Acute Disease; Aquaporins; Brain Edema; Chronic Disease; Humans; Hyponatremia; Hypovolemia; Vasopressins; Water-Electrolyte Imbalance