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PubMed2000

Oxytocin and vasopressin expression in the ovine testis and epididymis: changes with the onset of spermatogenesis.

Contractions of seminiferous tubules and epididymal duct walls promote spermiation and sperm transfer, and they are thought to be stimulated by the related peptides oxytocin and vasopressin. This study tested the hypothesis that if oxytocin and/or vasopressin play a physiological role in sperm shedding and transport, then local or circulating concentrations of these peptides would increase during puberty. Testes, epididymides, and trunk blood of sheep at stages during the first spermatogenic wave were collected, and radioimmunoassay measured significant increases in testicular and epididymal oxytocin during spermatogenesis. No changes were measured in circulating oxytocin or in local or circulating vasopressin. Localization and synthesis was investigated by immunohistochemistry and Western blot analysis employing antibodies recognizing epitopes of either oxytocin, oxytocin-associated neurophysin, vasopressin, or vasopressin-associated neurophysin. Marked expression of both oxytocin and its associated neurophysin in testicular Leydig and epididymal principal cells was seen, and weak neurophysin immunoreactivity was also identified in Sertoli cells. The intercellular distribution of oxytocin varied between regions of the epididymis, suggesting several roles for oxytocin. Vasopressin synthesis was not apparent in either tissue. These results confirm the presence and development of paracrine oxytocinergic systems in the ram testis and epididymis of ram during puberty while questioning the physiological importance of vasopressin.

Animals↗
PubMed1990

Endogenous vasopressin supports blood pressure and prevents severe hypotension during epidural anesthesia in conscious dogs.

To evaluate whether, and to what extent, release of endogenous vasopressin supports blood pressure when efferent sympathetic drive is blocked by epidural anesthesia, the authors studied the effects of high epidural anesthesia alone and when vasopressin was prevented from acting at its vascular (V1)-receptor in six awake, trained, unsedated dogs. On different days, the same dose of 0.5% bupivacaine (8-13 ml) was injected epidurally in a randomized fashion either in the presence or absence of (V1)-vasopressin receptor blockade, and the effects were evaluated on cardiovascular (arterial blood pressure, heart rate) and respiratory (blood gases, oxygen consumption) variables, and on plasma concentrations of vasopressin and renin. Results were also contrasted to those obtained after epidural injection of saline alone (placebo) in the same dogs. When endogenous vasopressin was prevented from acting by intravenous pretreatment with a specific V1-receptor antagonist (beta-mercapto-beta, beta-cyclopenta-methylene-propionyl-O-Me-Tyr-Arg-Vasopressin), epidural anesthesia resulted in a rapid and sustained 35% decrease in mean arterial blood pressure from 92 mmHg +/- 5 SE to 60 mmHg +/- 4. In contrast, only a 14% decrease in mean blood pressure from 92 mmHg +/- 5 to 79 mm Hg +/- 6 was noted after epidural anesthesia alone. This difference between groups was statistically significant (P = 0.0001). The V1-receptor blockade alone had no detectable effect. Vasopressin plasma concentrations significantly increased from 3.4 +/- 0.3 pg.ml-1 to 16.2 +/- 3.2 pg.ml-1 after epidural anesthesia but did not change after epidural saline.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Epidural↗
PubMed2002

Beneficial effects of short-term vasopressin infusion during severe septic shock.

BACKGROUND: Septic shock is associated with vasopressin deficiency and a hypersensitivity to its exogenous administration. The goal of the current study was to determine whether short-term vasopressin infusion in patients experiencing severe septic shock has a vasopressor sparing effect while maintaining hemodynamic stability and adequate end-organ perfusion. METHODS: Patients experiencing septic shock that required high-dose vasopressor support were randomized to a double-blinded 4-h infusion of either norepinephrine (n = 11) or vasopressin (n = 13), and open-label vasopressors were titrated to maintain blood pressure. To assess end-organ perfusion, urine output and creatinine clearance, gastric mucosal carbon dioxide tension, and electrocardiogram ST segment position were measured. RESULTS: Patients randomized to norepinephrine went from a median prestudy norepinephrine infusion of 20.0 microg/min to a blinded infusion of 17.0 mug/min at 4 h, whereas those randomized to vasopressin went from a median prestudy norepinephrine infusion of 25.0 microg/min to 5.3 microg/min at 4 h (P < 0.001). Mean arterial pressure and cardiac index were maintained in both groups. Urine output did not change in the norepinephrine group (median, 25 to 15 ml/h) but increased substantially in the vasopressin group (median, 32.5 to 65 ml/h; P < 0.05). Similarly, creatinine clearance did not change in the norepinephrine group but increased by 75% in the vasopressin group (P < 0.05). Gastric mucosal carbon dioxide tension and electrocardiogram ST segments did not change significantly in either group. CONCLUSIONS: The authors conclude that short-term vasopressin infusion spared conventional vasopressor use and improved some measures of renal function in patients with severe septic shock.

Aged↗
PubMed2001

Comparison of epinephrine with vasopressin on bone marrow blood flow in an animal model of hypovolemic shock and subsequent cardiac arrest.

OBJECTIVE: The intraosseous route is an emergency alternative for the administration of drugs and fluids if vascular access cannot be established. However, in hemorrhagic shock or after vasopressors are given during resuscitation, bone marrow blood flow may be decreased, thus impairing absorption of intraosseously administered drugs. In this study, we evaluated the effects of vasopressin vs. high-dose epinephrine in hemorrhagic shock and cardiac arrest on bone marrow blood flow. DESIGN: Prospective, randomized laboratory investigation that used an established porcine model for measurement of hemodynamic variables and organ blood flow. SETTING: University hospital laboratory. SUBJECTS: Fourteen pigs weighing 30 +/- 3 kg. INTERVENTIONS: Radiolabeled microspheres were injected to measure bone marrow blood flow during a prearrest control period and during hypovolemic shock produced by rapid hemorrhage of 35% of the estimated blood volume. In the second part of the study, ventricular fibrillation was induced; after 4 mins of untreated cardiac arrest and 4 mins of standard cardiopulmonary resuscitation, a bolus dose of either 200 microg/kg epinephrine (n = 6) or 0.8 units/kg vasopressin (n = 6) was administered. Defibrillation was attempted 2.5 mins after drug administration, and blood flow was assessed again at 5 and 30 mins after successful resuscitation. MEASUREMENTS AND MAIN RESULTS: Mean +/- sem bone marrow blood flow decreased significantly during induction of hemorrhagic shock from 14.4 +/- 4.1 to 3.7 +/- 1.8 mL.100 g-1.min-1 in the vasopressin group and from 18.2 +/- 4.0 to 5.2 +/- 1.0 mL.100 g-1.min-1 in the epinephrine group (p =.025 in both groups). Five minutes after return of spontaneous circulation, mean +/- sem bone marrow blood flow was 3.4 +/- 1.1 mL.100 g-1.min-1 after vasopressin and 0.1 +/- 0.03 mL.100 g-1.min-1 after epinephrine (p =.004 for vasopressin vs. epinephrine). At the same time, bone vascular resistance was significantly (p =.004) higher in the epinephrine group when compared with vasopressin (1455 +/- 392 vs. 43 +/- 19 mm Hg. mL-1.100 g.min, respectively). CONCLUSIONS: Bone blood flow responds actively to both the physiologic stress response of hemorrhagic shock and vasopressors given during resuscitation after hypovolemic cardiac arrest. In this regard, bone marrow blood flow after successful resuscitation was nearly absent after high-dose epinephrine but was maintained after high-dose vasopressin. These findings emphasize the need for pressurized intraosseous infusion techniques, because bone marrow blood flow may not be predictable during hemorrhagic shock and drug therapy.

Animals↗
PubMed2002

Depletion of neurohypophyseal content of vasopressin in septic shock.

OBJECTIVES: To assess the mechanisms underlying the inappropriately low plasma vasopressin levels reported in septic shock. DESIGN: Prospective case series. SETTING: A 26-bed general medical intensive care unit at a university hospital. PATIENTS: Septic shock patients. MEASUREMENTS AND MAIN RESULTS: In three consecutive patients with septic shock, plasma vasopressin levels, circulating vasopressinase activity, baroreflex sensitivity, and neurohypophyseal vasopressin content were assessed. Plasma vasopressin concentration was unexpectedly within normal range in two patients (1.6 pg/mL and 1.8 pg/mL) and increased in one (16 pg/mL). In all cases, vasopressinase activity was undetectable, baroreflex sensitivity was decreased, and the high signal intensity of the posterior lobe of the pituitary gland on T1-weighted magnetic resonance images was absent. Magnetic resonance imaging and plasma vasopressin levels normalized after recovery from shock in the patient who survived. CONCLUSION: These data suggest that in septic shock, inappropriately low plasma levels of vasopressin are at least partly related to a depletion of vasopressin stores in the neurohypophysis.

Aged↗
PubMed1999

Beneficial treatment of age-related sleep disturbances with prolonged intranasal vasopressin.

Disturbed sleep is common in the elderly and is characterized by disordered sleep architecture with reduced time spent in slow wave sleep (SWS) and in rapid eye movement (REM) sleep. At present, no treatments are available to fully compensate for these disorders. In the elderly, vasopressin content is decreased at various brain sites. Investigating the effects of a 3-month intranasal vasopressin administration on sleep and cognitive functions in two elderly subjects in a foregoing pilot study, the authors found that the most pronounced influence of the peptide was a marked increase in SWS. This placebo-controlled, double-blind, randomized study examined the influences of a 3-month period of daily intranasal vasopressin treatment (20 IU before bedtime and after awakening) on nocturnal sleep in 26 healthy elderly subjects (mean age, 74.2 years). Intranasal treatment of vasopressin increased (1) the total sleep time, on average, by 45 minutes (p < 0.002); (2) time spent in SWS by 21 minutes (p < 0.025); and (3) time in REM sleep in the second half of the night by 10 minutes (p < 0.01). Vasopressin promotes sleep time and improves sleep architecture after prolonged intranasal administration in elderly subjects, although scores of subjective sleep quality did not change. Results suggest that age-related deterioration of sleep architecture can benefit from intranasal treatment with vasopressin. But a potential use in clinical settings will also depend on demonstrating improved subjective sleep quality, which remained unaffected by vasopressin in this study of elderly subjects.

Administration, Inhalation↗
PubMed1988

Vasoconstrictor role of vasopressin and angiotensin in experimental aortic stenosis in the rat.

The roles of vasopressin and angiotensin II in the regulation of peripheral vascular tone were investigated in control rats and in rats with chronic (15 weeks) aortic stenosis, by intravenous application of a specific antagonist to the vascular receptors of vasopressin and the angiotensin-converting enzyme inhibitor teprotide. The application of a Silver clip (0.6 mm) on the aorta ascendens produced a hemodynamically effective aortic stenosis with an increase in left ventricular weight (38%), a reduction in mean arterial pressure, cardiac index, and stroke volume index, and an increase in peripheral vascular resistance. In both groups of rats, a bolus injection of 30 micrograms of the vasopressin inhibitor d (CH2) 5 Tyr (Me) arginine vasopressin (AVP) showed an agonistic effect by increasing arterial pressure by 11 and 15 mm Hg, respectively, and no antagonistic effect in the control animals. In the rats with chronic aortic stenosis we observed a significant fall in blood pressure (4.1 +/- 5.5 mm Hg; p less than 0.05) and a reduction in peripheral vascular resistance of 6.3% (p less than 0.02). Stroke volume index and heart rate did not change. Most of the animals with aortic stenosis had inappropriately elevated plasma levels of vasopressin and increased levels of plasma renin concentration. The rats with aortic stenosis and inappropriately increased values of vasopressin showed significantly lower plasma osmolality, cardiac index, and stroke volume index and increased peripheral vascular resistance compared with the stenosed rats with a normal osmoregulation of vasopressin.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II↗
PubMed2003

Arginine vasopressin, but not epinephrine, improves survival in uncontrolled hemorrhagic shock after liver trauma in pigs.

OBJECTIVE: Epinephrine is widely used for treatment of life-threatening hypotension, although new vasopressor drugs may merit evaluation. The purpose of this study was to determine the effects of vasopressin vs. epinephrine vs. saline placebo on hemodynamic variables, regional blood flow, and short-term survival in an animal model of uncontrolled hemorrhagic shock and delayed fluid resuscitation. DESIGN: Prospective, randomized, laboratory investigation that used a porcine model for measurement of hemodynamic variables and regional abdominal organ blood flow. SETTING: University hospital laboratory. SUBJECTS: A total of 21 pigs weighing 32 +/- 3 kg. INTERVENTIONS: The anesthetized pigs were subjected to a penetrating liver injury, which resulted in a mean +/- sem loss of 40% +/- 5% of estimated whole blood volume within 30 mins and mean arterial pressures of <20 mm Hg. When heart rate declined progressively, pigs randomly received a bolus dose and continuous infusion of either vasopressin (0.4 units/kg and 0.04 units.kg-1.min-1, n = 7), or epinephrine (45 microg/kg and 5 microg.kg(-1).min(-1), n = 7), or an equal volume of saline placebo (n = 7), respectively. At 30 mins after drug administration, all surviving animals were fluid resuscitated while bleeding was surgically controlled. MEASUREMENTS AND MAIN RESULTS: Mean +/- sem arterial blood pressure at 2.5 and 10 mins was significantly (p <.001) higher after vasopressin vs. epinephrine vs. saline placebo (82 +/- 14 vs. 23 +/- 4 vs. 11 +/- 3 mm Hg, and 42 +/- 4 vs. 10 +/- 5 vs. 6 +/- 3 mm Hg, respectively). Although portal vein blood flow was temporarily impaired by vasopressin, it was subsequently restored and significantly (p <.01) higher when compared with epinephrine or saline placebo (9 +/- 5 vs. 121 +/- 3 vs. 54 +/- 22 mL/min and 150 +/- 20 vs. 31 +/- 17 vs. 0 +/- 0 mL/min, respectively). Hepatic and renal artery blood flow was significantly higher throughout the study in the vasopressin group; however, no further bleeding was observed. Despite a second bolus dose, all epinephrine- and saline placebo-treated animals died within 15 mins after drug administration. By contrast, seven of seven vasopressin-treated animals survived until fluid replacement, and 60 mins thereafter, without further vasopressor therapy (p <.01). Moreover, blood flow to liver, gut, and kidney returned to normal values in the postshock phase. CONCLUSIONS: Vasopressin, but not epinephrine or saline placebo, improved short-term survival in a porcine model of uncontrolled hemorrhagic shock after liver injury when surgical intervention and fluid replacement was delayed.

Animals↗
PubMed2006

Serial circulating vasopressin levels in children with septic shock.

BACKGROUND: Septic shock is an important cause of death in pediatric intensive care units. Initial evaluations have shown that vasopressin may have a role in catecholamine refractory shock in adults. It is important to determine whether children with septic shock have deficiency of vasopressin. This will help in defining the role of vasopressin in septic shock. DESIGN: Prospective cohort study. SETTING: Pediatric intensive care unit of a tertiary care hospital in north India. PATIENTS: Patients were children with septic shock, and controls were children with sepsis but no shock. STUDY DESIGN: Vasopressin levels in plasma were determined by enzyme-linked immunosorbent assay for children with septic shock at diagnosis (baseline) and thereafter at 24, 48, and 96 hrs to determine the time trends. The baseline vasopressin values for children with septic shock were compared with those for children without shock. RESULTS: The median (95% confidence interval) vasopressin level at baseline in children with septic shock was 116 (63.3-130.7) pg/mL, and in children with sepsis but no shock it was 106 (61.7-131.77) pg/mL. The median value for survivors was 76 (44.6-130.9) pg/mL, and for nonsurvivors, 118 (81.7-259) pg/mL (p = .16). The serial values also did not show any significant changes; the values at 24 hrs (n = 17), 48 hrs (n = 16), and 96 hrs (n = 15) were 105 (76.1-125.9), 105 (41.4-155.5), and 109.5 (54.9-154.8) pg/mL, respectively. CONCLUSIONS: The results of our study suggest that vasopressin levels are elevated in children with septic shock and that serial values up to 96 hrs do not show any decline.

Chi-Square Distribution↗
PubMed2004

Regulatory mechanisms of corticotropin-releasing hormone and vasopressin gene expression in the hypothalamus.

Tuberoinfundibular corticotropin-releasing hormone (CRH) neurones are the principal regulators of the hypothalamic-pituitary-adrenal (HPA)-axis. Vasopressin is primarily a neurohypophysial hormone, produced in magnocellular neurones of the hypothalamic paraventricular and supraoptic nuclei, but parvocellular CRH neurones also coexpress vasopressin, which acts as a second 'releasing factor' for adrenocorticotropic hormone along with CRH. All stress inputs converge on these hypothalamic neuroendocrine neurones, and the input signals are integrated to determine the output secretion of CRH and vasopressin. Aminergic, cholinergic, GABAergic, glutamatergic and a number of peptidergic inputs have all been implicated in the regulation of CRH/vasopressin neurones. Glucocorticoids inhibit the HPA-axis activity by negative feedback. Interleukin-1 stimulates CRH and vasopressin gene expression, and is implicated in immune-neuroendocrine regulation. cAMP-response element-binding protein phosphorylation may mediate transcriptional activation of both CRH and vasopressin genes, but the roles of AP-1 and other transcription factors remain controversial. Expression profiles of the CRH and vasopressin genes are not uniform after stress exposure, and the vasopressin gene appears to be more sensitive to glucocorticoid suppression.

Animals↗
PubMed1986

Human platelet arginine vasopressin.

Approximately 90% of arginine vasopressin circulating in blood is associated with the platelets. Studies in six patients with cranial diabetes insipidus indicate that the platelet vasopressin originates in the hypothalamus and is taken up from plasma. Extracted platelet vasopressin is chromatographically identical to the posterior pituitary peptide and biologically active. Infusion of low-doses of exogenous vasopressin into 10 normal male subjects caused a marked rise in both plasma and platelet hormone concentrations. Stimulation of endogenous vasopressin release by hypertonic saline (0.51 mol/l) infusion for 135 min in five male subjects also caused a rise in platelet and plasma peptide concentrations. In seven male smokers, the deep inhalation of two consecutively smoked unfiltered cigarettes caused a significant rise in both platelet and plasma vasopressin. Baseline platelet vasopressin concentrations in the smokers were higher than in the non-smoking males even after 10 hours abstinence.

Adult↗
PubMed1991

The effect of a highly specific serotonin agonist on osmoregulated vasopressin secretion in healthy man.

OBJECTIVE: To explore a possible interaction of the serotonin neurotransmitter system and posterior pituitary function, we have looked at the effect of fluoxetine treatment on osmoregulated vasopressin secretion in normal men in two placebo controlled studies. DESIGN: In each study subjects took in random order for 7 days one capsule daily of placebo or 40 mg fluoxetine. On the 8th day subjects underwent assessment. Study 1 A hypo-osmotic stimulus of an oral water load of 20 ml/kg. Study 2 A hyperosmotic stimulus of intravenous infusion of 5% (855 mmol/l) saline at 0.06 ml/kg/min for 120 minutes. PATIENTS: Normal, healthy male volunteers. Study 1, 9; Study 2, 10. MEASUREMENTS: In both studies regular measures of plasma osmolality, sodium and vasopressin were made. In Study 1 urine osmolality was measured together with urine volume at set time points and an accumulative measure of percentage of water load excreted. Free water clearance was calculated. In Study 2 the relationship of plasma vasopressin to change in plasma osmolality was calculated for each subject by linear regression analysis. RESULTS: Serotonin agonism had no effect on baseline measurements in either study. Study 1 After 4 hours subjects excreted 95 and 99% of the water load after placebo and fluoxetine respectively (P = 0.407). There was no effect of fluoxetine compared to placebo on the pattern or extent of change of plasma osmolality (nadir 285.9 +/- 1.4 mosm/kg placebo, 283.1 +/- 1.1 mosm/kg fluoxetine, P = 0.145) or free water clearance or maximum urine dilution after oral water loading. Plasma vasopressin suppressed to a minimum concentration after both treatments in response to hypo-osmolality 0.5 +/- 0.1 pmol/l (placebo), 0.3 +/- 0.01 pmol/l (fluoxetine), P = 0.195. Study 2 Fluoxetine had no significant effect on the sensitivity of vasopressin release to change in plasma osmolality (0.33 +/- 0.06 pmol/l per mosm/kg placebo, 0.36 +/- 0.06 pmol/l per mosm/kg fluoxetine, P = 0.347). Nor was there a significant effect on the theoretical osmotic threshold for release of vasopressin (287.0 +/- 1.21 mosm/kg placebo, 286.9 +/- 1.09 mosm/kg fluoxetine, P = 0.700). CONCLUSION: We have found no evidence of a physiologically relevant effect of serotonin agonism on osmoregulated vasopressin release, or on the ability of normal man to excrete a water load. The possible reasons for this contrast to animal work are discussed.

Adolescent↗
PubMed1995

Antisense vasopressin oligonucleotides: uptake, turnover, distribution, toxicity and behavioral effects.

The uptake, turnover, distribution, toxicity and behavioral effects of antisense vasopressin oligonucleotides were investigated to define how these compounds interact with neural tissue to inhibit translation of a target mRNA. Both phosphorothioate modified and unmodified oligonucleotides are rapidly taken up by mammalian neural tissue. Turnover of the unmodified oligonucleotide was found to be fast (t1/2 < 1 h) relative to the phosphorothioate modified oligonucleotide (t1/2 = 12 h). The phosphorothioate vasopressin antisense oligonucleotide suppressed vasopressin synthesis in vivo at concentrations below the toxic threshold of approximately 5 microM. Intracranial injections of phosphorothioate antisense oligonucleotide into the region of the SON in vivo, resulted in a small decrease in vasopressin mRNA and a compensatory drinking response within the first 24 h, consistent with a deficit in vasopressin translation with kinetics similar to those observed in vitro. Water intake returned to normal by the second day indicating relatively rapid clearance of the oligonucleotide and minimal side effects. Although the mechanisms of accumulation and details of the molecular interactions are still unknown, our observation of preferential uptake and/or retention of oligonucleotide within a subset of neurons in vitro suggests some process of selective targeting. Thus, low concentrations of oligonucleotides targeted to the untranslated 5' end of vasopressin mRNA can be effective for the acute and reversible control of vasopressin synthesis in mammalian CNS with relatively rapid onset of behavioral effects and minimal side effects.

Animals↗
PubMed1988

Effect of pH on vasopressin-induced water permeability in collecting ducts of isolated rat papillae.

1. The effects of basolateral and luminal pH on diffusional water permeability of microperfused collecting ducts of isolated rat papillae were examined in the presence and absence of vasopressin at two concentrations. 2. In the absence of vasopressin, collecting duct diffusional water permeabilities did not differ when the pH of the luminal fluid was varied. Similarly, in the absence of vasopressin, collecting duct diffusional water permeabilities did not differ when the bath pH was varied. 3. In the presence of 50 microU/ml vasopressin, increases in diffusional water permeability of collecting ducts perfused with solutions at pH 5.0, 7.4 or 9.0 did not differ significantly. Similarly, increases in diffusional water permeability induced by 200 microU/ml vasopressin were not different when collecting ducts were perfused with solutions at pH 5.0, 7.4 or 9.0. 4. The presence of vasopressin (50 microU/ml) in the bathing medium at pH 6.4, 7.4 and 8.4 induced increments in diffusional water permeability of 0.40 +/- 0.21 (n = 14, P greater than 0.05), 1.56 +/- 0.27 (n = 27, P less than 0.001) and 1.67 +/- 0.24 (n = 12, P less than 0.001) microns/s, respectively. The increment in water permeability at pH 6.4 was significantly less than that at pH 7.4 (P less than 0.001). 5. The presence of vasopressin (200 microU/ml) in the bathing medium at pH 6.4, 7.4 and 8.4 induced increments in diffusional water permeability of 2.16 +/- 0.54 (n = 9, P less than 0.01), 2.55 +/- 0.51 (n = 17, P less than 0.001) and 0.98 +/- 0.34 (n = 11, P less than 0.05) microns/s respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Vasopressin response to haemorrhage in rats: effect of hypoxia and water restriction.

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

Animals↗
PubMedDate not supplied

A controlled study of glypressin versus vasopressin in the control of bleeding from oesophageal varices.

To evaluate the therapeutic effect of glypressin (triglycyl-lysine-vasopressin, C52H74N16O15S2.2C2H4O2.5H2O) in the treatment of oesophageal variceal bleeding, a randomized controlled trial of glypressin and vasopressin was conducted in 54 cirrhotic patients with oesophageal varices bleeding. Bleeding ceased within 24 h in 50% (13/26) of patients treated with glypressin and in 53.6% (15/28) of patients given vasopressin. Re-bleeding within 7 days occurred in 30.8% (4/13) of the glypressin group and in 20.0% (3/15) of the vasopressin group. There was no statistically significant difference in the therapeutic effect between glypressin and vasopressin. In the glypressin group, bleeding was more easily stopped in non-hepatocellular carcinoma (HCC) cirrhotic patients of Pugh's criteria A or B than in patients of Pugh's criterion C or HCC. We conclude that glypressin and vasopressin have similar therapeutic effect. In considering the application convenience, glypressin is an alternative to vasopressin in the treatment of bleeding varices in patients of good liver function reserve.

Carcinoma, Hepatocellular↗
PubMed2005

Cardiopulmonary resuscitation with vasopressin in a dog.

That endogenous vasopressin levels in successfully resuscitated human patients were significantly higher than in patients who died pointed to the possible benefit of administering vasopressin during cardiopulmonary resuscitation (CPR). Several CPR studies in pigs showed that vasopressin improved blood flow to vital organs, cerebral oxygen delivery, resuscitability and neurological outcome when compared with epinephrine. In a small clinical study, vasopressin significantly improved short-term survival when compared with epinephrine indicating its potential as an alternative pressor to epinephrine during CPR in human beings. As there was little clinical data available at that time, its recommended use was limited to adult human beings with shock-refractory ventricular fibrillation. In this report, we present the case of a dog in which the successful management of intraoperative asystolic cardiac arrest involved vasopressin. Unexpected cardiac arrest occurred during anaesthesia for the surgical removal of multiple mammary adenocarcinomata in a 11-year-old Yorkshire terrier. Despite an ASA physical status assignation of III, the dog was successfully resuscitated with external chest compressions, intermittent positive pressure ventilation and vasopressin (2 doses of 0.8 IU kg(-1)) and was discharged 3 days later without signs of neurological injury. We believe vasopressin contributed to restoring spontaneous circulation. It may prove increasingly useful in perioperative resuscitation in dogs.

Anesthesia↗
PubMed2000

Adolescent stress and neural plasticity in hamsters: a vasopressin-serotonin model of inappropriate aggressive behaviour.

Animal studies show that arginine vasopressin facilitates aggression, while serotonin (5-HT) inhibits aggression by blocking the activity of the vasopressin system. Clinical studies report that subjects with a history of 'fighting and assault' show a significant positive correlation between cerebrospinal fluid concentrations of vasopressin and aggression in the presence of a hyporeactive 5-HT system. Thus, in animals and humans, a hyporeactive 5-HT system may result in enhanced vasopressin activity and increased aggression. Can the stress of emotional and physical insult, i.e. threat and attack, during adolescence affect the development of the vasopressin and 5-HT systems and alter normal aggressive behaviour in early adulthood? Adolescent male golden hamsters were weaned at postnatal day 25, and stressed for 2 weeks by daily 1 h bouts of threat and attack by adult hamsters. Male littermates were run in a parallel stress study using daily 1 h trials of isolation in a novel environment. During early adulthood, on postnatal day 45, 3 days after the cessation of stress trials, animals were tested for aggression in a resident: intruder model. The results show a context-dependent change in aggression. Animals with a history of abuse show exaggerated attack behaviour toward smaller males compared to littermates with a history of isolation stress. Conversely, when confronted by males of equal size, animals with a history of abuse show diminished aggression and increased submission compared to controls. It was determined that the density of vasopressin fibres and neurones in the hypothalamus is lower in abused animals compared to controls. In contrast, the number of 5-HT terminals within the hypothalamus is higher in abused animals compared to controls. These results provide evidence in an animal model that stress in the form of threat and attack during adolescence can alter the balance between vasopressin and 5-HT in the brain, resulting in inappropriate aggressive behaviour in early adulthood.

Aggression↗