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PubMed1985

Ca2+-dependent activation of oxoglutarate dehydrogenase by vasopressin in isolated hepatocytes.

Vasopressin stimulated gluconeogenesis from proline in hepatocytes from starved rats; this was attributed to an activation of oxoglutarate dehydrogenase (EC 1.2.4.2) [Staddon & McGivan (1984) Biochem. J. 217, 477-483]. The role of Ca2+ in the activation mechanism was investigated. (1) In the absence of extracellular Ca2+, vasopressin caused a stimulation of gluconeogenesis and a decrease in cell oxoglutarate content that were markedly transient when compared with the effects in the presence of Ca2+. (2) Ca2+ added to cells stimulated for 2 min by vasopressin in the absence of extracellular Ca2+ sustained the initial effects of vasopressin. Ca2+ added 15 min after vasopressin, a time at which both the rate of gluconeogenesis and the cell oxoglutarate content were close to the control values, caused a stimulation of gluconeogenesis and a decrease in cell oxoglutarate content. (3) Under conditions of cell-Ca2+ depletion, vasopressin had no effect on gluconeogenesis or cell oxoglutarate content. (4) Ionophore A23187 stimulated gluconeogenesis and caused a decrease in cell oxoglutarate content, but the phorbol ester 4 beta-phorbol 12-myristate 13-acetate had no effects. (5) These data suggest that the initial activation of oxoglutarate dehydrogenase by vasopressin is dependent on an intracellular Ca2+ pool and independent of extracellular Ca2+. For activation of a greater duration, a requirement for extracellular Ca2+ occurs. The activation of oxoglutarate dehydrogenase by A23187 is consistent with a mechanism involving Ca2+, but the lack of effect of 4 beta-phorbol 12-myristate 13-acetate indicates that protein kinase C is not involved in the mechanism of activation by vasopressin.

Animals↗
PubMed1991

Reduced oxygen consumption induced by vasopressin in dogs depends on systemic administration.

1. Arginine vasopressin reduces whole-body oxygen consumption in conscious dogs. To determine whether this decrease could result from limited oxygen delivery, studies were performed in two groups of chronically instrumented dogs. 2. In the first group (n = 7), vasopressin was infused at a rate of 18.5 pmol min-1 kg-1 while the animals were breathing 10% oxygen. Hypoxaemia alone (arterial partial pressure of oxygen 4.67 kPa) decreased whole-body oxygen delivery by 30%. The fall in whole-body oxygen consumption induced by vasopressin during hypoxaemia was not different from that measured under normoxic conditions, even though whole-body oxygen delivery was more reduced. 3. In a second group of seven dogs, hindquarter blood flow (electromagnetic flowmeter on lower abdominal aorta) and oxygen consumption (blood flow multiplied by arteriovenous oxygen difference) were measured as infusions of vasopressin were given either systemically or into the lower abdominal aorta. Systemic vasopressin infusions at 0.92, 4.6 and 18.5 pmol min-1 kg-1 reduced hindquarter blood flow, oxygen delivery and oxygen consumption, but the decreases in blood flow and oxygen delivery were dose-related whereas that in oxygen consumption was not. Intra-arterial infusions of vasopressin that increased venous concentrations as much as or more than systemic infusion of 0.92 pmol of vasopressin min-1 kg-1 had no effect on oxygen consumption, even though the higher intra-arterial rate reduced blood flow and oxygen delivery as much as the systemic infusion. Thus systemic but not locally administered vasopressin reduced hindquarter oxygen consumption.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Renal, haemodynamic and hormonal interactions between atrial natriuretic factor and arginine vasopressin in patients with congestive heart failure.

1. Nine patients with compensated heart failure were infused with synthetic arginine vasopressin at a rate of 0.1 m-units min-1 kg-1 for 60 min to increase their plasma arginine vasopressin concentration. Synthetic human atrial natriuretic factor (3 pmol min-1 kg-1) or placebo was co-infused with the arginine vasopressin in random order in a single-blind cross-over design. 2. The resultant plasma concentrations of arginine vasopressin and atrial natriuretic factor fell to within the upper range observed in congestive heart failure. Compared with the infusion of arginine vasopressin alone, atrial natriuretic factor co-infusion enhanced both the urine flow rate and the sodium excretion rate (both P less than 0.05) without significant haemodynamic and hormonal effects. 3. Systematic blood pressure was elevated by arginine vasopressin infusion (P less than 0.05) without any change in heart rate. Co-infusion of atrial natriuretic factor did not affect these haemodynamic parameters. 4. These results suggest that an increased release of atrial natriuretic factor maintains water and sodium excretion in the presence of arginine vasopressin-induced renal modulations, and that the pressor effect of arginine vasopressin is not antagonized by the increased plasma level of atrial natriuretic factor in patients with congestive heart failure.

Aged↗
PubMed1992

Metabolic clearance rate of arginine vasopressin in severe chronic renal failure.

1. The metabolic clearance rate of arginine vasopressin was determined using a constant infusion technique in normal subjects and patients with chronic renal failure immediately before commencing dialysis. Endogenous arginine vasopressin was suppressed in all subjects before the infusion with a water load. 2. Plasma arginine vasopressin concentrations were determined using a sensitive and specific radioimmunoassay after Florisil extraction. The detection limit of the assay was 0.3 pmol/l, and intra- and inter-assay coefficients of variation at 2 pmol/l were 9.7% and 15.3%, respectively. 3. In normal subjects, the metabolic clearance rate was determined at two infusion rates producing steady-state concentrations of arginine vasopressin of 1.3 and 4.4 pmol/l. In the patients with renal failure, a single infusion rate was used, producing a steady-state concentration of 1.5 pmol/l. 4. At comparable plasma arginine vasopressin concentrations, metabolic clearance rate was significantly reduced in patients with renal failure (normal 1168 +/- 235 ml/min versus renal failure 584 +/- 169 ml/min; means +/- SD; P < 0.001). 5. Free water clearance was significantly reduced in normal subjects during the arginine vasopressin infusion from 8.19 +/- 2.61 to -1.41 +/- 0.51 ml/min (P < 0.001), but was unchanged in the patients with renal failure after attaining comparable plasma arginine vasopressin concentrations. 6. In normal subjects there was a small but significant fall in metabolic clearance rate at the higher steady-state arginine vasopressin concentration (1168 +/- 235 ml/min at 1.3 pmol/l versus 1059 +/- 269 ml/min at 4.4 pmol/l; P = 0.016).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1995

Effect of dietary salt restriction on renal sensitivity to vasopressin in man.

1. We have previously described a progressive antidiuresis in response to low-dose vasopressin infusion during salt restriction in man, despite stable or even declining plasma vasopressin concentration. In the present study we examine the hypothesis that renal sensitivity to the antidiuretic effect of arginine vasopressin may be enhanced by salt restriction. 2. Extremely low-dose infusions of arginine vasopressin were given to normal subjects after equilibration to high (260 mmol/day) and low (20 mmol/day) sodium intakes. 3. Salt restriction increased the antidiuretic effect of arginine vasopressin (2 fmol min-1 kg-1 arginine vasopressin increased urine osmolality from 67.8 +/- 2.6 to 196.3 +/- 35.7 mosmol/l in the high-salt study and from 268.3 +/- 49 mosmol/l in the low-salt study; P < 0.05 between sodium intakes). Glomerular filtration rate, estimated from inulin clearance, was unchanged during arginine vasopressin infusion irrespective of salt intake (high salt 116.5 +/- 9.4 to 118.9 +/- 6.4 ml/min; low salt, 135.1 +/- 9.2 to 111.2 +/- 12.4 ml/min). Renal plasma flow, estimated from para-aminohippurate clearance, fell further during infusion of 2 fmol min-1 kg-1 arginine vasopressin in the low-salt study than in the high-salt study (low salt, from 555.7 +/- 22.7 to 298.3 +/- 27.6 ml/min; high salt, from 544.5 +/- 30.2 to 452.9 +/- 28.9 ml/min; P < 0.05 between sodium intakes).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1998

Effects of receptor blockade on metabolism and renal actions of vasopressin in conscious dogs.

Vasopressin--but not the V2 receptor agonist [deamino-cis1,D-Arg8]-vasopressin (dDAVP)--may mediate natriuresis in dogs. The present study investigated this phenomenon by use of nonpeptide antagonists to V1a and V2 receptors 1-¿1-[4-(3-acetylaminopropoxy)benzoyl]-4-piperidyl¿-3,4-dihydro-2 (1H)-quinolinone (OPC-21268) and 5-dimethylamino-1-¿4-(2-methylbenzoylamino)-benzoyl¿-2,3,4,5-tetra hydro-1 H-benzazepine (OPC-31260), respectively) hypothesising that only V1a inhibition would reduce the natriuresis. In conscious dogs vasopressin secretion was suppressed by water loading (2% body weight) and replaced by infusion of vasopressin (50 pg min-1 kg-1) resulting in physiological plasma concentrations (plasma levels of AVP (pAVP) = 2.0 +/- 0.1 pg mL-1). In this setting, OPC-21268 did not change the rate of sodium excretion. OPC-31260 increased water excretion 12-fold without significant changes in sodium excretion. Heart rate, mean arterial blood pressure, glomerular filtration rate, and clearance of endogenous Li+ were unchanged. During vasopressin infusion, both antagonists increased pAVP, OPC-21268 by 20% and OPC-31260 by 100% (2.0 +/- 0.2-4.0 +/- 0.3 pg mL-1). In the absence of vasopressin infusion, OPC-31260 did not increase pAVP. Thus, the increase in pAVP appeared to be due to a decrease in metabolic clearance rate. The results indicate that the present dose of V1a receptor inhibitor OPC-21268 does not reduce sodium excretion and that both vasopressin antagonists inhibit vasopressin metabolism.

Animals↗
PubMed2003

Histamine and prostaglandin interaction in regulation of oxytocin and vasopressin secretion.

Prostaglandins and histamine in the hypothalamus are involved in the regulation of oxytocin and vasopressin secretion, and appear to be involved in the mediation of pituitary hormone responses to immunochallenges. Therefore, we investigated in conscious male rats: (i) whether blockade of H1 or H2 receptors affected the oxytocin and vasopressin responses to prostaglandins and (ii) whether blockade of prostaglandin synthesis affected the oxytocin and vasopressin responses to histamine or to Escherichia coli lipopolysaccharide (LPS), in order to determine any interaction between prostaglandins and histamine in the hypothalamus. Oxytocin secretion was dose-dependently stimulated by intracerebroventricular infusion of 1 or 5 microg of PGE1, PGE2 or PGF2alpha, with PGE2 being the most potent of the compounds used. Prior central infusion of the H1 receptor antagonist mepyramine or the H2 receptor antagonist cimetidine significantly inhibited the oxytocin response to all three prostaglandins by approximately 50%. Vasopressin secretion was increased by PGE1 but not by PGE2 or PGF2alpha. The stimulatory effect of PGE1 was almost annihilated by prior administration of mepyramine or cimetidine. Central infusion of histamine or immunochallenge with LPS administered intraperitoneally increased oxytocin and vasopressin secretion four- and two-fold, respectively. Pretreatment with systemic injection of the prostaglandin synthesis inhibitor indomethacin dose-dependently reduced the oxytocin response and prevented the vasopressin response to histamine or LPS. We conclude that histamine and PGE1, PGE2 or PGF2alpha interact in the regulation of oxytocin secretion, whereas histamine and only PGE1 interact in the regulation of vasopressin secretion. Furthermore, histamine as well as LPS may affect oxytocin and vasopressin neurones via activation of prostaglandins, probably in the hypothalamic supraoptic nucleus.

Animals↗
PubMed2000

A simplified index of the plasma sodium threshold for arginine vasopressin secretion-morning fasting, euhydrated sodium levels.

OBJECTIVE: Human pregnancy results in a reduction in plasma osmolality and thus a reduction in the osmotic threshold for arginine vasopressin secretion. Although the functional characteristics of the osmoregulatory system controlling arginine vasopressin secretion have been carefully defined, determination of the osmotic threshold requires a complex, labor-intensive protocol of an intravenous hypertonic saline infusion. To aid in studies of osmotic threshold resetting in pregnancy, we sought to develop a simplified method for determination of this value. STUDY DESIGN: Ten healthy nonpregnant women between the ages of 18 and 40 years were studied over 2 days. All patients were hospitalized, and morning euhydration was ensured by oral water hydration (5-10 mL/kg) the evening before the study. On the first study day, patients were fed a standard no-salt-added diet; plasma osmolality and sodium values were checked just before and 1 and 2 hours after meals. On the second study day, after fasting blood samples were obtained, patients received an intravenous infusion (0.06 mL. kg(-1). min(-1) for 120 minutes) of hypertonic (5%) saline to gradually increase the plasma sodium level. Blood samples were obtained every 15 minutes for measurement of plasma electrolytes and arginine vasopressin. Plasma arginine vasopressin concentrations were regressed against plasma osmolality and sodium concentration to calculate the osmotic threshold for arginine vasopressin secretion. RESULTS: Hypertonic saline injection significantly increased plasma sodium (from 139 +/- 1 to 149 +/- 1 mEq/L) and osmolality (from 284 +/- 2 to 304 +/- 2 mOsm/kg H(2)O). Plasma arginine vasopressin significantly increased (from 5 +/- 1 to 30 +/- 10 pg/mL). The mean sodium and osmolality thresholds for arginine vasopressin secretion were calculated as 137 +/- 2 mEq/L and 285 +/- 15 mOsm/kg H(2)O. The mean morning fasting sodium level was nearly identical to the calculated sodium threshold, whereas the morning fasting osmolality value was significantly different. CONCLUSIONS: The morning fasting, euhydrated sodium level can be used as a simplified index for the plasma osmotic threshold for arginine vasopressin secretion. This index may provide a useful predictive measure for pregnant women in whom the plasma volume does not expand.

Adolescent↗
PubMed2003

Vasopressin type 1A receptor up-regulation by cyclosporin A in vascular smooth muscle cells is mediated by superoxide.

Based on our previous results, we investigated whether cyclosporin A (CsA)-induced vasopressin type 1A receptor up-regulation was mediated by free radicals. We report that CsA analogues with different affinities for cyclophilin and calcineurin were able to up-regulate vasopressin type 1A receptor and to generate free radicals in smooth muscle cells independently of calcineurin. Further, we demonstrate that the antioxidant N-acetyl-L-cysteine blocked the increase in vasopressin type 1A receptor mRNA and protein levels induced by CsA and that low concentrations of prooxidants were able to directly increase vasopressin type 1A receptor mRNA and protein levels. In addition, short exposure to CsA or pro-oxidants was sufficient to significantly increase vasopressin type 1A receptor mRNA and protein levels. Using cell-permeable forms of superoxide dismutase and catalase, we finally show that superoxide mediates the CsA-induced effects on vasopressin type 1A receptor. These results provide strong evidence that CsA-induced superoxide generation is causally involved in vasopressin type 1A receptor expression and demonstrate for the first time that low physiological concentrations of radicals, most probably superoxide, are able to directly affect cellular signaling to increase vasopressin type 1A receptor expression in rat aortic smooth muscle cells.

Animals↗
PubMed2003

Short-term stimulation of the renal Na-K-Cl cotransporter (NKCC2) by vasopressin involves phosphorylation and membrane translocation of the protein.

Na-K-Cl cotransporter (NKCC2)-mediated sodium chloride reabsorption in the thick ascending limb is stimulated by the antidiuretic hormone vasopressin. We investigate the mechanisms underlying the short term activation of NKCC2 by vasopressin in vivo, finding that administration of a vasopressin analogue (deamino-Cys-d-Arg vasopressin) causes a 2-fold increase in mouse kidney NKCC2 phosphorylation, as detected with a phosphospecific antibody, R5. The subtissue localization of the activation is defined by immunofluorescence. In vasopressin-treated animals, a dramatic increase in R5 immunostaining is observed in the initial segment of the thick ascending limb located in the inner stripe of the outer medulla, the region with a higher sensitivity to vasopressin. Although a pool of NKCC2 is present in cytoplasmic vesicles, the distribution of the phosphorylated cotransporter seems to be restricted to the cell membrane compartment; morphometric analysis of electron microscope images demonstrates a 55% increase in NKCC2 molecules at the apical membrane, suggesting the administration of vasopressin induces trafficking of the cotransporter. Thus, the short term actions of vasopressin on the thick ascending limb cotransporter are mediated by both an effect on the translocation of the protein and an increase in phosphorylation of regulatory threonines in the amino terminus of NKCC2.

Animals↗
PubMed1996

Role of vasopressin in altered pial artery responses to dynorphin and beta-endorphin following brain injury.

Pial artery constriction following fluid percussion brain injury (FPI) is associated with elevated CSF dynorphin and beta-endorphin concentration in newborn pigs. Additionally, dynorphin is a dilator under control conditions and a vasoconstrictor under decreased cerebrovascular tone conditions. Vasopressin contributes to beta-endorphin-induced pial constriction and the constrictor potential for dynorphin. Recently, it has been observed that FPI reverses vasopressin from a dilator to a constrictor. The present study was designed to characterize the effect of FPI on beta-endorphin-induced constriction and the role of vasopressin in that constriction as well as in the reversal of dynorphin's vascular response following FPI. Brain injury of moderate severity (1.9 - 2.3 atm) was produced in anesthetized newborn pigs equipped with a closed cranial window. Dynorphin in physiologic and pharmacologic concentrations (10(-10), 10(-8), 10(-6) M) was reversed from a dilator to a constrictor following FPI (7 +/- 1, 11 +/- 1, and 16 +/- 1 vs -4 +/- 1, -7 +/- 1, and -11 +/- 1% before and after FPI, respectively). Dynorphin-induced vascular changes were accompanied by increased cortical periarachnoid CSF vasopressin and these biochemical changes were potentiated following FPI (24 +/- 4 vs 134 +/- 7 and 53 +/- 7 vs 222 +/- 14 pg/mliter for control and dynorphin (10(-6) M) before and after FPI, respectively). In contrast, in animals pretreated with the vasopressin receptor antagonist [1-(beta-mercapto-beta beta-cyclopentamethylene propionic acid) 2-(O-methyl)-Tyr-AVP] (MEAVP, 5 micrograms/kg iv), dynorphin-induced constriction following FPI was attenuated (6 +/- 1, 12 +/- 1, and 16 +/- 1, vs -2 +/- 1, -4 +/- 1, and -7 +/- 1% before and after FPI, respectively). Additionally, beta-endorphin-induced pial constriction was potentiated following FPI (-7 +/- 1, -10 +/- 1, -15 +/- 1 vs -10 +/- 1 -15 +/- 2, and -21 +/- 2% for beta-endorphin (10(-10), 10(-8), 10(-6) M) before and after FPI, respectively). beta-endorphin-induced CSF vasopressin release was similarly potentiated following FPI. Further, MEAVP blunted the augmented constrictor responses to beta-endorphin observed following FPI (-5 +/- 1, -9 +/- 1, -14 +/- 1 vs -2 +/- 1, -5 +/- 1, and -8 +/- 1% before and after FPI, respectively). These data indicate that FPI potentiates beta-endorphin-induced pial construction and reverses dynorphin from a dilator to a constrictor. Additionally, these data show that vasopressin contributes to augmented beta-endorphin pial constriction and the reversal of dynorphin's vascular effects following FPI. Further, since CSF dynorphin and beta-endorphin concentrations are increased following FPI, these data suggest that these two opioids contribute to pial artery constriction observed following FPI, at least, in part, via the release of vasopressin.

Animals↗
PubMed1999

The effects of intrinsic vasopressin on urinary aquaporin-2 excretion and urine osmolality during surgery under general anesthesia.

UNLABELLED: A radioimmunoassay has been established to measure urinary aquaporin-2 excretion (u-AQP2). To elucidate how u-AQP2 changes when endogenous vasopressin is increased independently of plasma osmolality, we estimated u-AQP2 during general anesthesia for surgery. We collected urine and blood samples from 50 patients before and 90 and 180 min after anesthetic induction. Plasma (29.1+/-12.6 pg/mL) and urinary (565.1+/-207.0 ng/gCr) vasopressin levels were markedly increased after anesthetic induction. Although no significant alteration of plasma osmolality or serum sodium concentration was observed during 180 min, u-AQP2 was significantly increased (preinduction 224.5+/-24.2 fmol/ mgCr; 90 min 243.3+/-31.8; 180 min 331.4+/-45.9), paralleling an increase of plasma and urinary vasopressin. The plasma vasopressin concentration after anesthetic induction was far in excess of that expected based on plasma osmolality. Individual plasma and urinary vasopressin concentrations correlated significantly with u-AQP2. At 180 min after anesthesia, plasma osmolality did not change, but urine osmolality decreased despite increased u-AQP2, and a preanesthetic positive correlation between urine osmolality and u-AQP2 disappeared. Thus, although u-AQP2 correlates with increased intrinsic vasopressin levels, the increase in u-AQP2 did not directly contribute to urine concentration. Apparently, an escape from the physiologic effects of high vasopressin level occurs during anesthesia via a mechanism independent of aquaporin-2. We conclude that the anesthetic would interfere with the urinary concentrating capacity at the level of AQP2-action. IMPLICATIONS: The excessive increase of intrinsic vasopressin exactly augmented urinary aquaporin-2 excretion, resulting in urine concentration; however, anesthesia seemed to modify this process possibly by interfering with the aquaporin-2 action.

Adolescent↗
PubMed2000

Vasopressin improves survival after cardiac arrest in hypovolemic shock.

UNLABELLED: Survival after hypovolemic shock and cardiac arrest is dismal with current therapies. We evaluated the potential benefits of vasopressin versus large-dose epinephrine in hemorrhagic shock and cardiac arrest on vital organ perfusion, and the likelihood of resuscitation. In 18 pigs, 35% of the estimated blood volume was withdrawn over 15 min and ventricular fibrillation was induced 5 min later. After 4 min of cardiac arrest and 4 min of standard cardiopulmonary resuscitation, a bolus dose of either 200 microg/kg epinephrine (n = 7), 0.8 unit/kg vasopressin (n = 7), or saline placebo (n = 4) was administered in a blinded, randomized manner. Defibrillation was attempted 2.5 min after drug administration, and all animals were subsequently observed for 1 h without further intervention. Spontaneous circulation was restored in 7 of 7 vasopressin animals, in 6 of 7 epinephrine pigs, and in 0 of 4 placebo swine. At 5 and 30 min after return of spontaneous circulation, median (minimum and maximum) renal blood flow after epinephrine was 2 (0-31), and 2 (0-48) mL. 100 g(-1). min(-1), respectively; and after vasopressin 96 (12-161), and 44 (16-105) mL. 100 g(-1). min(-1), respectively (P: <.01 between groups). Epinephrine animals developed a profound metabolic acidosis by 15 min after return of spontaneous circulation (mean arterial pH, 7.11 +/- 0.01), and by 60 min all epinephrine-treated animals had died. The vasopressin pigs had (P: = 0.015) less acidosis (pH = 7.26+/-0. 04) at corresponding time points, and all survived > or =55 min (P: < 0. 01). In conclusion, treatment of hypovolemic cardiac arrest with vasopressin, but not with large-dose epinephrine or saline placebo, resulted in sustained vital organ perfusion, less metabolic acidosis, and prolonged survival. Based on these findings, clinical evaluation of vasopressin during hypovolemic cardiac arrest may be warranted. IMPLICATIONS: The chances of surviving cardiac arrest in hemorrhagic shock are considered dismal without adequate fluid replacement. However, treatment of hypovolemic cardiac arrest with vasopressin, but not with large-dose epinephrine or saline placebo, resulted in sustained vital organ perfusion and prolonged survival in an animal model of suspended infusion therapy.

Animals↗
PubMed2001

The efficacy of epinephrine or vasopressin for resuscitation during epidural anesthesia.

Cardiopulmonary resuscitation (CPR) during epidural anesthesia is considered difficult because of diminished coronary perfusion pressure. The efficacy of epinephrine and vasopressin in this setting is unknown. Therefore, we designed this study to assess the effects of epinephrine versus vasopressin on coronary perfusion pressure in a porcine model with and without epidural anesthesia and subsequent cardiac arrest. Thirty minutes before induction of cardiac arrest, 16 pigs received epidural anesthesia with bupivacaine while another 12 pigs received only saline administration epidurally. After 1 min of untreated ventricular fibrillation, followed by 3 min of basic life-support CPR, Epidural Animals and Control Animals randomly received every 5 min either epinephrine (45, 45, and 200 microg/kg) or vasopressin (0.4, 0.4, and 0.8 U/kg). During basic life-support CPR, mean +/- SEM coronary perfusion pressure was significantly lower after epidural bupivacaine than after epidural saline (13 +/- 1 vs 24 +/- 2 mm Hg, P < 0.05). Ninety seconds after the first drug administration, epinephrine increased coronary perfusion pressure significantly less than vasopressin in control animals without epidural block (42 +/- 2 vs 57 +/- 5 mm Hg, P < 0.05), but comparably to vasopressin after epidural block (45 +/- 4 vs 48 +/- 6 mm Hg). Defibrillation was attempted after 18 min of CPR. After return of spontaneous circulation, bradycardia required treatment in animals receiving vasopressin, especially with epidural anesthesia. Systemic acidosis was increased in animals receiving epinephrine than vasopressin, regardless of presence or absence of epidural anesthesia. We conclude that vasopressin may be a more desirable vasopressor for resuscitation during epidural block because the response to a single dose is longer lasting, and acidosis after multiple doses is less severe compared with epinephrine.

Anesthesia, Epidural↗
PubMed1997

Impaired microvascular vasoconstrictive responses to vasopressin in septic rats.

OBJECTIVE: To evaluate mechanisms of vasodilation in sepsis by comparing responses of resistance arterioles to vasopressin in rat cremaster muscle of septic and control rats. DESIGN: Prospective, experimental study. SETTING: Experimental animal laboratory. SUBJECTS: Twenty male rats, anesthetized with ketamine and acepromazine. INTERVENTIONS: Topical superfusion of vasoactive compounds on skeletal muscle resistance arterioles. MEASUREMENTS AND MAIN RESULTS: The effect of sepsis on responses to local application of vasopressin was investigated using in vivo videomicroscopy. Vasopressin was superfused topically on the cremaster muscle resistance arterioles (15 to 25 microns) of rats made septic by cecal ligation and puncture, and the responses were compared with the responses of controls that underwent sham ligation. Responses to topically suffused vasopressin were also assessed in septic and control rats, before and after superfusion of the muscle with the nitric oxide synthase inhibitor NG-methyl-L-arginine (NMA). Sepsis produced a decrease in the vasoconstrictive effects of vasopressin; the maximal response was lower, and the concentration-response curve was shifted to the right in septic rats (p < .05). Contractions at vasopressin concentrations of 0.01, 1, and 10 nM were 39%, 36%, and 40%, respectively, of sham controls. Superfusion of the muscle with NMA partially restored arteriolar responsiveness in the septic rats, significantly increasing the arteriolar constriction of the septic rats in response to vasopressin. This effect was reversed with superfusion of excess L-arginine (1 mM). CONCLUSIONS: This study illustrates the reduced responsiveness of the resistance arterioles of septic rats in response to vasopressin in vivo, and the partial restoration of responsiveness by concurrent application of NMA. In previous studies using this model, we have shown similar results using norepinephrine and endothelin-1, as well as angiotensin II. These findings, and the findings of this study, suggest a generalized abnormality in responsiveness of resistance arterioles to endogenous vasoconstrictors in sepsis. Partial reversal of this abnormality with NMA supports an important role for nitric oxide in mediating abnormal vasopressor responsiveness in sepsis.

Animals↗
PubMed2000

Vasopressin-mediated adrenocorticotropin release increases plasma cortisol concentrations during cardiopulmonary resuscitation.

OBJECTIVE: Vasopressin is a possible stimulus for both adrenocorticotropin (ACTH) and endothelin-1 release. The aim of this study was to compare plasma concentrations of ACTH, cortisol, and endothelin-1 after epinephrine or vasopressin administration in an experimental animal model of cardiopulmonary resuscitation (CPR). DESIGN: Prospective, randomized, controlled animal study. SETTING: A university research laboratory. SUBJECTS: Fourteen 12- to 14-wk-old domestic pigs. INTERVENTIONS: After 4 mins of cardiac arrest and 3 mins of external chest compression, the pigs were randomly assigned to receive either 0.045 mg/kg epinephrine (n = 7) or 0.4 units/kg vasopressin (n = 7). At 5 mins after drug administration, defibrillation was attempted. MEASUREMENTS AND MAIN RESULTS: Coronary perfusion pressure, ACTH, cortisol, and endothelin-1 were measured before cardiocirculatory arrest, during CPR before drug administration, and at 90 secs and 5 mins after drug administration. Coronary perfusion pressure was comparable between groups. All seven animals in the vasopressin group survived, but only one pig in the epinephrine group survived (p = .005). ACTH and cortisol concentrations remained unchanged in epinephrine-treated animals, but increased significantly after vasopressin administration and were significantly higher than in epinephrine-treated animals 5 mins after drug administration. Endothelin-1 concentrations remained unchanged during the study period and were comparable between both groups. CONCLUSIONS: Vasopressin is a potent stimulus for ACTH secretion, but does not trigger endothelin-1 release from vascular cells during cardiac arrest and CPR. The increased plasma cortisol concentrations caused by the enhanced ACTH release after vasopressin may be one factor contributing to the improved outcome repeatedly observed with vasopressin in animal models of CPR.

Adrenocorticotropic Hormone↗
PubMed1999

Effects of deamino-8-D-arginin vasopressin on blood loss and coagulation factors in scoliosis surgery. A double-blind randomized clinical trial.

STUDY DESIGN: A double-blind, randomized, prospective clinical study was performed to evaluate the efficacy of deamino-8-D-arginin vasopressin in reducing blood loss in major scoliosis surgery. OBJECTIVES: To evaluate whether desmopressin has any effect on reducing blood loss in spinal surgery, to identify the probable mechanisms of effectiveness via blood coagulation factors, and to outline any adverse effect associated with the use of deamino-8-D-arginin vasopressin. SUMMARY OF BACKGROUND DATA: Scoliosis surgery is known to be associated with major blood loss. Because of major drawbacks of homologous blood transfusion, many alternative methods have been used to counter the blood loss. Only a few studies exist, with controversial results, on the use of deamino-8-D-arginin vasopressin. METHODS: The study population included 40 operations on 35 consecutive patients undergoing reconstructive surgery for either idiopathic (n = 26) or congenital (n = 9) scoliosis. Operations were randomized into deamino-8-D-arginin vasopressin (0.3 microgram/kg body weight; maximum, 20 micrograms) (n = 18) or placebo (n = 22) groups and stratified according to the diagnosis and the type of surgery performed (i.e., anterior versus posterior versus anterior and posterior sequential). Parameters of blood loss, serum levels of blood coagulation factors at different time intervals, and urinary output were measured. RESULTS: Findings indicated that blood loss per kilogram of body weight, blood loss per surgically treated spinal level, urinary output per kilogram of body weight and serum levels of fibrinogen, von Willebrand factor (vWF) activity, tissue type plasminogen activator activity, and plasminogen activator inhibitor activity were not sensitive to the administration of deamino-8-D-arginin vasopressin at any time interval during surgery or at 24 hours after surgery (P > 0.05). Only factor VIII:C levels exhibited significant elevations at 30 minutes and at 24 hours (P < 0.05). CONCLUSIONS: This study could not demonstrate any significant effect of deamino-8-D-arginin vasopressin on the amount of blood loss in a group of patients with idiopathic or congenital scoliosis. Findings indicate that for most of the coagulation factors, any changes in serum levels induced by deamino-8-D-arginin vasopressin were much like those expected from surgery itself. This study also failed to demonstrate any significant effects altering the urinary output that may be attributed to the use of deamino-8-D-arginin vasopressin.

Adolescent↗
PubMed2004

Heterogeneity of the vasoconstrictor effect of vasopressin in septic shock.

OBJECTIVE: To determine whether pressor doses of vasopressin impair organ blood flow in endotoxic shock. DESIGN: Graded doses of vasopressin or phenylephrine, starting at the clinically recommended doses for pressure support in septic shock, were intravenously infused during endotoxic shock. SETTING: University hospital surgical research laboratory. SUBJECTS: Twelve random-bred female Yorkshire pigs. INTERVENTIONS: We measured mean arterial pressure, cardiac output, heart rate, pulmonary artery occlusion pressure, and carotid, mesenteric, renal, and iliac blood flows. MEASUREMENTS AND MAIN RESULTS: Low doses of vasopressin (typically used in the clinical management of septic shock) raised arterial pressure by increasing systemic vascular resistance without a significant preferential effect in the circulations measured. However, moderately greater doses of vasopressin had a very heterogeneous vasoconstrictor action; although there was no significant vasoconstriction in the carotid and iliac circulations, mesenteric and renal blood flows decreased markedly. Furthermore, at pressor doses vasopressin improved cerebral perfusion. CONCLUSIONS: The vasoconstrictor action of exogenous low-dose vasopressin in endotoxic shock does not impair blood flow to any of the vascular beds examined. However, moderately higher doses of vasopressin may induce ischemia in the mesenteric and renal circulations. The data indicate that the safe dose range for exogenous vasopressin in septic shock is narrow and support the current practice of fixed low-dose administration, generally 0.04 units/min and in no case exceeding 0.1 units/min.

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