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PubMed2004

A comparison of epinephrine and vasopressin in a porcine model of cardiac arrest after rapid intravenous injection of bupivacaine.

UNLABELLED: In a porcine model, we compared the efficacy of epinephrine, vasopressin, or the combination of epinephrine and vasopressin with that of saline placebo on the survival rate after bupivacaine-induced cardiac arrest. After the administration of 5 mg/kg of a 0.5% bupivacaine solution i.v., ventilation was interrupted for 3 +/- 1 min (mean +/- SD) until asystole occurred. Cardiopulmonary resuscitation (CPR) was initiated after 1 min of cardiac arrest. After 2 min of CPR, 28 animals received, every 5 min, epinephrine; vasopressin; epinephrine combined with vasopressin; or placebo i.v.. Three minutes after each drug administration, up to 3 countershocks (3, 4, and 6 J/kg) were administered; all subsequent shocks were 6 J/kg. Blood was drawn throughout the experiment for the determination of plasma bupivacaine concentration. In the vasopressin/epinephrine combination group, all pigs survived (P < 0.01 versus placebo); in the vasopressin group 5 of 7, in the epinephrine group 4 of 7, and in the placebo group none of 7 swine survived. The plasma concentration of total bupivacaine showed no significant difference among groups. In this model of bupivacaine-induced cardiac arrest, CPR with a combination of vasopressin and epinephrine resulted in significantly better survival rates than in the placebo group. IMPLICATIONS: Although cardiovascular collapse occurs mostly immediately after rapid injection of a local anesthetic in the presence of anesthesiologists, resuscitation may be difficult, and the outcome is usually poor. In this model of bupivacaine-induced cardiac arrest, cardiopulmonary resuscitation with a combination of vasopressin and epinephrine resulted in significantly better survival rates than in the placebo group.

Anesthetics, Local↗
PubMed1981

The importance of vasopressin in the mechanism maintaining hypertension in the rat.

The further role of vasopressin in the pathogenesis of hypertension was studied in two different types of hypertensive rats in which the intravenous injection of a vasopressin antiserum reduced arterial blood pressure substantially. The increased secretion of vasopressin was demonstrated in deoxycorticosterone acetate (DOCA)-salt hypertensive and spontaneously hypertensive rats with high salt intake. Angiotensin II binding of the brain receptor which has been postulated to modify osmotically stimulated vasopressin release from neurohypophysis was not affected by sodium balance in these types of hypertensive rats, whereas the decrease in the brain receptor binding of angiotensin II was observed in the control rats. The lack of the adjusting control system in the brain angiotensin II receptors for sodium balance may be, at least in a part, responsible for the enhancement of vasopressin secretion in the hypertensive rats compared to that in the control rats with high salt intake. Since pressor responsiveness to vasopressin was increased in the rats with DOCA-salt hypertension, vasopressin may function as a direct pressor agent in the maintenance of high blood pressure in this type of hypertension.

Angiotensin II↗
PubMed1995

Effect of moderately increased intrapelvic pressure on renal tissue pressure and vasopressin release in rabbits.

Electrical stimulation of afferent renal nerves and activation of intrarenal receptors increases plasma vasopressin concentration, but the role of afferent renal nerves in the control of vasopressin secretion is not clear. Recently, we reported that activation of renal mechanoreceptors stimulates the release of vasopressin. However, intrapelvic pressure was increased to 50 mmHg, and this increase is above the normal physiological range. Therefore, in the present study, we investigated the effect of moderately increased intrapelvic pressure on plasma vasopressin concentration in anesthetized rabbits. First, we measured renal tissue pressure while intrapelvic pressure was increased stepwise in 10-mmHg increments. Basal renal tissue pressure was 17 +/- 2 mmHg. Renal tissue pressure increased only when intrapelvic pressure was higher than the basal tissue pressure of each animal. Usually, increases in intrapelvic pressure less than 20 mmHg did not increase renal tissue pressure. This finding suggests that only increases in intrapelvic pressure more than 20 mmHg can activate renal mechanoreceptors. Based on this finding, the effects of moderate increases in intrapelvic pressure (15 and 30 mmHg) were studied. With a 15-mmHg increase in intrapelvic pressure, plasma vasopressin concentration did not change significantly. However, when intrapelvic pressure was increased to 30 mmHg, plasma vasopressin concentration increased from 5.6 +/- 1.4 to 9.5 +/- 2.8 pg/ml at 5 min (p < 0.05) and to 8.8 +/- 2.0 pg/ml at 10 min (p < 0.05). Plasma renin activity and mean arterial pressure also increased when intrapelvic pressure was increased to 30 mmHg. We conclude that moderate increases in intrapelvic pressure stimulate vasopressin secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1979

[A comparison between the effects of angiotensin II and angiotensin III injected into the third cerebral ventricle on vasopressin secretion in conscious rats (author's transl)].

As the greater part of the immunoreactive angiotensin II in cerebrospinal fluid has been suggested to be angiotensin III, a comparison was made between the effects on vasopressin release of angiotensin II and angiotensin III administered into the third cerebral ventricle in conscious male rats. The blood samples were collected 90 seconds after the injection of angiotensin II or angiotensin III by means of decapitation. Plasma vasopressin (microU/ml) extracted and determined by radioimmunoassay were 2.3 +/- 0.8, 6.7 +/- 5.0, 14.0 +/- 2.2, 16.3 +/- 4.3 and 20.7 +/- 2.5 (mean +/- SEM), respectively following the injection of 0, 10, 25, 50 and 100ng of angiotensin II. The increases in plasma vasopressin produced by angiotensin II 25, 50 and 100ng were statistically significant (p less than 0.05). On the other hand, plasma vasopressin following the injection of 22.7 and 45.4ng of angiotensin III, which are equimolar to 25 and 50ng of angiotensin II each, were 14.9 +/- 2.7 and 16.3 +/- 5.6, respectively. No significant difference was found between the effect on plasma vasopressin of angiotensin II and that of angiotensin III at the dose level of 24.3 or 48.6 p. mol. These data indicate that angiotensin III is equipotent to angiotensin II in terms of vasopressin release when administered into the third cerebral ventricle. The possible role of angiotensin III in the brain on vasopressin secretion is discussed.

Angiotensin II↗
PubMed1989

Pathophysiology of vasopressin in edematous disorders.

Sodium and water retention is characteristic of edematous disorders including cardiac failure, cirrhosis, nephrotic syndrome and pregnancy. In recent years the use of a sensitive radioimmunoassay for plasma vasopressin has implicated the role of nonosmotic vasopressin release in the water retention of these edematous disorders. In experimental studies and studies in humans it has been found that the nonosmotic release of vasopressin is consistently associated with activation of the sympathetic nervous and renin-angiotensin-aldosterone systems. Moreover, the sympathetic nervous system has been shown to be involved in the nonosmotic release of vasopressin (carotid and aortic baroreceptors) and activation of the renin-angiotensin system (renal beta-adrenergic receptors). These findings have led to our proposal that body fluid volume regulation involves the dynamic interaction between cardiac output and peripheral arterial resistance. In this context neither total extracellular fluid (ECF) volume nor blood volume are determinants of renal sodium and water excretion. Rather, renal sodium and water retention is initiated by either a fall in cardiac output (e.g. ECF volume depletion, low-output cardiac failure, pericardial tamponade or hypovolemic nephrotic syndrome) or peripheral arterial vasodilation (e.g. high-output cardiac failure, cirrhosis, pregnancy, sepsis, arteriovenous fistulae and pharmacologic vasodilators). With a decrease in effective arterial blood volume (EABV), initiated by either a fall in cardiac output or peripheral arterial vasodilation, the acute response involves vasoconstriction mediated by angiotensin, sympathetic mediators and vasopressin. The slower response to restoring EABV involves vasopressin-mediated water retention and aldosterone-mediated sodium retention. The renal vasoconstriction which accompanies those states that decrease EABV, by either decreasing cardiac output or causing peripheral arterial vasodilation, limits the distal tubular delivery of sodium and water thus maximizing the water-retaining effect of vasopressin and impairing the normal escape from the sodium-retaining effects of aldosterone. The elevated glomerular filtration rate and filtered sodium load in pregnancy allows increased distal sodium and water delivery in spite of a decrease in EABV, thus limiting edema formation during gestation.

Blood Volume↗
PubMed1978

Effect of vasopressin on intracranial pressure of rabbit.

Effect of vasopressin on intracranial pressure (ICP) was examined by an intraventricular administration of the hormone to a rabbit. ICP was determined at the cisterna magna with a manometer and recorded automatically with a recorder. An injection of over 150 micro U of vasopressin lowered ICP, but there was no clear dose-response relationship of the effect of vasopressin on ICP. When vasopressin was injected intraventricularly after lowering ICP by an intravenous injection of acetazolamide which inhibits the production of cerebrospinal fluid (CSF), an additive effect of the hormone on ICP was observed. The effect of vasopressin on excretion of water in CSF was examined by the determination of drainage of tritiated water injected into the lateral ventricle of a rabbit. Drainage of radioactive water into vein was measured by collection of blood at the internal jugular vein and radioactivity of the plasma was counted. Vasopressin accelerated excretion of tritiated water into vein. These results indicate that vasopressin facilitated drainage of CSF into vein to lower ICP.

Acetazolamide↗
PubMed1986

The neurohypophyseal hormones vasopressin and oxytocin. Precursor structure, synthesis and regulation.

Complete cDNA sequences for the vasopressin and oxytocin precursor polyproteins have been determined for the rat, calf, human and pig (vasopressin only), indicating the essential conservation of the precursor structures throughout mammals. DNA probes specific for vasopressin or oxytocin mRNAs have been used to identify both classic (hypothalamic) and novel (thymus, corpus luteum, phaeochromocytoma) sites of hormone expression. Semiquantitative DNA/RNA hybridization suggests that in rats expression of the vasopressin and oxytocin genes is positively effected by osmotic stress, negatively by a systemically applied excess of vasopressin; in the latter experiment a reduction in the hypothalamic levels of vasopressin and oxytocin mRNAs in normal and Brattleboro rats have been observed. This suggests a feedback regulation by the hormone as a possible element in controlling the transcription of the vasopressin gene.

Animals↗
PubMed1977

High vasopressin concentrations in human umbilical cord blood--lack of correlation with stress.

Marked elevations in the vasopressin concentrations in human umbilical cord blood have been reported previously (4, 8). This could either be a part of generalized increase in the activity of fetal endocrine system at the time of birth, a phenomenon that has led to the concept of fetal participation in the onset of labor, or simply due to the stress of delivery. The present study is an attempt to examine the later possibility. Plasma vasopressin was determined by radioimmunoassay [9] in separately collected arterial and venous blood from the umbilical cords of 24 babies spontaneously delivered and 14 babies born after Caesarian Section in the absence of labor. Arterial acid-base determinations were done in each case. The Apgar Score was evaluated by one individual. In order to obtain a general idea of circulating concentration of this hormone in the neonatal period, vasopressin concentrations were determined in the systemic venous blood of 12 normal and 10 stressed babies. Vasopressin concentrations in the umbilical arterial blood of babies born after spontaneous delivery were remarkably high, as compared to all the other groups. Despite a wide range, between 5-2200 pg/ml, there was no correlation between the magnitude of vasopressin elevation and the severity of fetal asphyxia (Fig. 1). The present finding in part, confirms and expands previously observed increased vasopressin levels in the cord blood after spontaneous vaginal delivery. In addition, a lack of correlation between fetal asphyxia and the vasopressin levels suggests that these high levels may not be related to this form of stress.

Acid-Base Equilibrium↗
PubMed1982

Effects of orchidectomy and sex steroids on vasopressin response to dehydration.

The secretion of vasopressin has been shown recently to be influenced by gonadal steroids. To further evaluate the relevance of sex steroids in the control of vasopressin secretion, the vasopressin response to dehydration has been studied in normal, castrated and sex-steroid treated castrated male rats. Short-term (3 weeks) castration did not modify the vasopressin response to 48 h of water deprivation. Long-term (10 weeks) castration, on the other hand, consistently reduced the vasopressin response by more than 50%. In both cases, the osmolality was unaffected. Treatment of long-term castrated rats with testosterone, dihydrotestosterone, or oestradiol increased the vasopressin response to dehydration towards normal control levels. However, only oestradiol could restore it to and beyond normal levels, although all three steroids were given in doses that were equipotent in bringing back to normal the plasma LH levels of the castrated animals. Angiotensin-II generation may indirectly be augmented by oestradiol treatment and this may account for the effect of oestradiol here reported. No such mechanism, however, may be invoked in the case of androgens; a direct modulatory effect at the hypothalamic level is postulated for explaining their influence on vasopressin secretion.

Age Factors↗
PubMed1994

Centrally administered vasopressin modifies stress hormone (cortisol, prolactin) secretion in sheep under basal conditions, during restraint and following intravenous corticotrophin-releasing hormone.

The effects of central (lateral ventricle) injections of vasopressin (2.5, 25 or 250 ng) on cortisol and prolactin release were investigated in castrated male sheep (N = 6) under basal (non-stress) conditions, during 120min of physical restraint and following peripheral injection of ovine corticotrophin-releasing hormone (oCRH). Cortisol and prolactin concentrations in non-stressed sheep were raised significantly (p < 0.05) in the 120 min following administration of 250 ng of vasopressin. The prolactin response to restraint stress was decreased (p < 0.05) in the 30-min period following central injection of 250 ng of vasopressin. The stimulatory effect of oCRH on cortisol release was enhanced (p < 0.05) by vasopressin (25 and 250 ng), whereas prolactin levels decreased (p < 0.02) in the 30-min period following injection of the highest dose of vasopressin. None of the central doses of vasopressin significantly altered plasma levels of this hormone, although vasopressin secretion was increased during restraint.

Animals↗
PubMed2004

Transient diabetes insipidus after discontinuation of therapeutic vasopressin.

The use of vasopressin for the treatment of septic shock is increasing. Few reports of fluid and electrolyte complications of this therapy have been reported. A neurologically impaired, 53-year-old man with a history of syndrome of inappropriate antidiuretic hormone developed apparent transient diabetes insipidus and acute hypernatremia after being treated with vasopressin. He was treated for presumed septic shock with intravenous vasopressin 0.01-0.10 U/minute. His blood pressure did not improve with this therapy, and his course was complicated by hyponatremia during the vasopressin infusion. Discontinuation of the infusion was followed by a profound (8.4 L) diuresis and rapid onset of hypernatremia (serum sodium concentration increased from 132 to 157 mEq/L over 8 hrs). Although urine osmolality was not measured during the patient's diuresis, the rapid changes in serum sodium concentration can be explained only by an inappropriate water diuresis. The diuresis ceased when the vasopressin infusion was resumed. We concluded that these findings are most consistent with transient diabetes insipidus. The safety and efficacy of intravenous vasopressin have not been established in patients with septic shock and underlying disorders of water homeostasis. The drug may have diminished vasoconstrictive effects in this patient population. Careful monitoring of water and sodium balance is warranted in all patients treated with vasopressin for septic shock.

Acute Disease↗
PubMed1990

Vasopressin responses to hypoxia in conscious rats: interaction with water restriction.

The purpose of this study was to determine the effect of water restriction on the vasopressin response to hypoxia in conscious Long-Evans rats. Rats were prepared with chronic indwelling femoral artery and vein catheters 1 week before experimentation. At 24 h before the first blood sample, the supply of drinking water was maintained ad libitum (water replete) or removed (water deplete). At 24 h, a control blood sample was taken and then normoxia (21% O2) was maintained or hypoxia (10% O2) induced. Additional blood samples were taken at 1, 18 and 24 h. All blood samples (2.5 ml) were simultaneously replaced with donor blood to maintain isovolaemia. Hypoxia led to a very small and transient increase in vasopressin in the water-replete rats. The combination of hypoxia and water restriction led to a greatly augmented vasopressin response at 1 h (60 +/- 16 pmol/l); this response was also not sustained. Additional non-cannulated rats were exposed to 24 h of normoxia or hypoxia with or without water available ad libitum and posterior pituitaries were collected after decapitation for measurement of vasopressin content. Water restriction, hypoxia and water restriction plus hypoxia all led to decreased pituitary vasopressin content. We conclude that the vasopressin response to hypoxia in conscious rats is small and transient, and that concomitant water restriction augments the vasopressin response to acute but not chronic hypoxia.

Animals↗
PubMed1992

A comparison of plasma vasopressin and oxytocin concentrations during the oestrous cycle of the ewe.

Blood samples were collected twice daily (09.30 and 17.00 h) via indwelling jugular-vein cannulae from five ewes throughout an entire oestrous cycle. Additional frequent samples were taken at 30-min intervals for 8 h on each of days 3 (early luteal phase), 9 (midluteal phase), 12 (late luteal phase) and 0 (day of oestrus). Plasma concentrations of arginine vasopressin and oxytocin were measured in all samples by radioimmunoassay and progesterone was measured in the twice-daily samples only. Both oxytocin and progesterone showed the expected pattern of plasma concentrations, increasing during the early luteal phase, reaching a plateau and declining either preceding (oxytocin) or at (progesterone) luteolysis. Vasopressin concentrations showed a significant dependence on the day of cycle (P less than 0.05, analysis of variance) with concentrations lowest at oestrus and minor peaks on days 4 and 8-9. There was no correlation between the concentrations of vasopressin and progesterone. Vasopressin values were significantly higher in the morning than in the afternoon samples (1.3 cf. 0.9 pmol/l; P less than 0.001). Analysis of the frequent samples showed a significant (P less than 0.001) dependence on the time of day for vasopressin but not oxytocin. Values were high throughout the morning, declined to a trough at 15.00 h and rose again by 17.00 h. We conclude that there is a minor variation in the vasopressin concentration during the oestrous cycle, which is not related to the circulating progesterone concentration but could be regulated by oestradiol. We also provide evidence for a diurnal rhythm in the release of vasopressin into the plasma in the ewe.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Plasma and urinary levels of vasopressin in enuretic and non-enuretic children.

Plasma and urinary levels of vasopressin were measured by radioimmunoassay in 18 children with primary nocturnal enuresis and 20 age and sex matched controls. All subjects followed a protocol whereby all urine were collected and divided up into daytime (8 a.m.-8 pm) and night-time (8 p.m. - 8 a.m.) samples. Urine osmolality and urinary vasopressin levels were measured and, following an overnight observation period, the following morning (8 a.m.) plasma vasopressin was measured. Plasma vasopressin was significantly lower in the enuretic group (2.86 +/- 0.44 pg/ml) compared to the control group (3.64 +/- 1.35 pg/ml) (p = 0.011). Total urinary vasopressin excretion over 24 hours was lower in the enuretic group but the difference was not significant. These results support the hypothesis that one of the factors responsible for nocturnal enuresis in children may be due to a reduced nocturnal secretion of vasopressin. This may explain why the vasopressin substitution therapy is able to successfully abolish nocturnal enuresis symptoms.

Adolescent↗
PubMed1984

Chronic effects of norepinephrine and vasopressin on urinary prostaglandin E and kallikrein excretions in conscious rats.

To assess in vivo functional interactions of vasopressor substances, norepinephrine and vasopressin, with renal prostaglandins and kallikrein-kinin system which are responsible for the vasodepressor mechanism in the kidney, we evaluated chronic effects of norepinephrine (1.8 mg/kg/day ip) and vasopressin (7.2 U/kg/day ip) on urinary prostaglandin E excretion and urinary kallikrein excretion in conscious rats. Both norepinephrine and vasopressin induced a sustained increase in systolic blood pressure. Norepinephrine induced slight but significant increases in urinary prostaglandin E excretion and urinary kallikrein excretion which were sustained for up to 6 days. Vasopressin induced a marked increase in urinary prostaglandin E excretion which was sustained for up to 6 days, whereas it induced a sustained decrease in urinary kallikrein excretion. Circulating angiotensin II levels was not changed by norepinephrine, but was decreased by vasopressin. These results indicate that renal prostaglandin E may not correlate with renal kallikrein-kinin and renin-angiotensin system in the responses to norepinephrine and vasopressin, and that vasopressin may be a more potent stimulator of the synthesis or release of renal prostaglandin E.

Angiotensin II↗
PubMed1997

Remodeling of capillary network in left ventricular subendocardial tissues induced by intravenous vasopressin administration.

OBJECTIVE: The question of whether the coronary vasospasm induced by intravenous administration of vasopressin produces any remodeling of the capillary network in the left ventricle was investigated. To this end, cardiac tissues obtained from vasopressin-injected rats were stained to allow capillary counting and for basic fibroblast growth factor (bFGF). METHODS: Nine male Donryu rats were divided into three groups that received, respectively, 0.25 ml of saline containing 0, 0.5, or 1.0 U/kg vasopressin injected into the tail vein once daily for 4 days. Rats were killed 30 days after the last injection. Two additional rats each received a single intravenous injection of 1.0 U/kg vasopressin and were killed 24 hours later. The left ventricles were removed and 16- or 10-micron frozen sections were cut for differential staining and distribution of bFGF, respectively. Differential staining was used to classify the capillary portions, and bFGF was identified by immunohistological staining. RESULTS: Compared with the control group, total capillary density was increased in both vasopressin-treated groups, capillary to myocyte ratio was increased, and the capillary domain areas decreased in the three capillary portions. Arteriolar and intermediate capillary portions increased, while the venular capillary portion decreased. In rats killed 24 hours after vasopressin injection, a considerable amount of bFGF could be demonstrated immunohistochemically in the ventricular tissues, and the punctate distribution of bFGF was still found in rats killed 30 days after treatment. CONCLUSIONS: A remodeling of capillary network which would increase the oxygen transport capacity to cardiac tissues was produced in left ventricular tissues by intravenous injection of vasopressin. bFGF located around capillaries and in the interstitial space may have been involved in the capillary remodeling.

Animals↗
PubMed1996

Vasopressin administration in refractory cardiac arrest.

BACKGROUND: Successful outcomes after cardiopulmonary resuscitation remain disappointingly infrequent, in animal studies, administration of exogenous vasopressin during closed- and open-chest cardiopulmonary resuscitation has recently been shown to be more effective than optimal doses of epinephrine in improving vital organ blood flow. OBJECTIVE: To describe the clinical effects and outcomes of administering vasopressin to patients in cardiac arrest refractory to current medical therapies. DESIGN: Case reports. SETTING: University hospital. PATIENTS: 8 adults with in-hospital cardiac arrest. INTERVENTIONS: After intravenous epinephrine (administered according to American Heart Association guidelines) and defibrillation efforts had failed, patients in cardiac arrest who were having cardiopulmonary resuscitation received 40 U of vasopressin intravenously and then defibrillation. MEASUREMENTS: Return of spontaneous circulation and hospital discharge rates. RESULTS: After administration of vasopressin, spontaneous circulation was promptly restored in all patients. Three patients were discharged from the hospital with intact neurologic function; the other five lived for between 30 minutes and 82 hours. CONCLUSION: In the presence of ventricular fibrillation with severe hypoxia and acidosis, vasopressin seems to be more potent and effective than adrenergic vasopressors for restoring spontaneous cardiovascular function. These results do not justify the widespread use of vasopressin for refractory cardiac arrest. However, on the basis of these cases, further studies comparing vasopressin with epinephrine are warranted in an effort to improve the currently dismal prognosis of patients after cardiac arrest.

Adult↗
PubMed1976

The effect of vasopressin on renal function in young rats a clearance and micropuncture study.

Using micropuncture techniques, the author studied the effect of vasopressin on renal function in young rats at three stages of development -- in the middle of the weaning period (22 days), after weaning was over (30 days) and at the beginning of the sexual maturation period (42 days). In the presence of a hypotonic load, a small dose of vasopressin (12 muU/100 g b.w., i.v.) was most effective in the youngest age group, where it reduced the urine flow by 82% both by increasing water reabsorption and by reducing the GFR. In this group, vasopressin lowered the TF/P Na+ ratio and raised the TF/P K+ ratio in the initial part of the distal tubules of the superficial nephrons, but raised water absorption only beyond the initial part of the distal tubules. Vasopressin reduced the urine flow by 72% in 30-day-old rats by raising water reabsorption beyond the initial part of the distal tubules. The only ion to be affected was K+, whose concentration rose in the final urine. In 42-day-old rats the effect of vasopressin was manifested in only mild depression of the GFR. In this age group, as distinct from younger animals, anaesthesia and surgery evidently led to endogenous vasopressin release, so that the small dose of exogenous vasopressin did not significantly influence the test parameters. This is also underlined by the significant difference between the control urine flow of the 42-day-old and the younger rats.

Age Factors↗