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We investigated intestinal oxygen supply and mucosal tissue [Po.sub.2] during administration of increasing dosages of continuously infused arginine vasopressin (AVP) in an autoperfused, innervated jejunal segments in anesthetized pigs. Mucosal tissue [Po.sub.2] was measured by employing two Clark-type surface oxygen electrodes. Oxygen saturation of jejunal microvascular hemoglobin was determined by tissue reflectance spectrophotometry. Microvascular blood flow was assessed by laser-Doppler velocimetry. Systemic hemodynamic variables, mesenteric venous and systemic acid-base and blood gas variables, and lactate measurements were recorded. Measurements were performed at baseline and at 20-min intervals during incremental AVP infusion (n = 8; 0.007, 0.014, 0.029, 0.057, 0.114, and 0.229 IU*[kg.sup.-1]*[h.sup.-1], respectively) or infusion of saline (n = 8). AVP infusion led to a significant (P < .05), dose-dependent decrease in cardiac index (from 121 [+ or -] 31 to 77 [+ or -] 27 m1*[kg.sup.-1].min-1 at 0.229 IU*[kg.sup.-1]*[h.sup.-1]) and systemic oxygen delivery (from 14 [+ or -] 3 to 9 [+ or - ]3 m1*[kg.sup.-1]*[min.sup.-1] at 0.229 IU*[kg.sup.-1]*[h.sup.-1]) concomitant with an increase in systemic oxygen extraction ratio (from 31 [+ or -] 4 to 48 [+ or -] 10%). AVP decreased microvascular blood flow (from 133 [+ or -] 47 to 82 [+ or -] 35 perfusion units at 0.114 IU*[kg.sup.-1]*[h.sup.-1]), mucosal tissue [Po.sub.2] (from 26 [+ or -] 7 to 7 [+ or -] 2 mmHg at 0.229 IU*[kg.sub.-1]*[h.sub-1]), and microvascular hemoglobin oxygen saturation (from 51 [+ or -] 9 to 26 [+ or -] 12% at 0.229 IU*[kg.sup.-1]*[h.sup.-1]) without a significant increase in mesenteric venous lactate concentration (2.3 [+ or -] 0.8 vs. 3.4 [+ or -] 0.7 mmol/1). We conclude that continuously infused AVP decreases intestinal oxygen supply and mucosal tissue [Po.sub.2] due to a reduction in microvascular blood flow and due to the special vascular supply in the jejunal mucosa in a dose-dependent manner in pigs. mucosal oxygen delivery; microcirculatory blood flow; Clark-type surface oxygen electrodes; reflectance spectrophotometry; jejunum

Background.Brain tissue oxygen pressure (PbtO2) correlates to cerebral blood flow (CBF) during spontaneous circulation, with one important regulator being nitric oxide (NO). Although it is established that arginine vasopressin (AVP) improves CBF and global cerebral oxygenation during cardiopulmonary resuscitation, it is unknown whether similar beneficial effects are present during spontaneous circulation. The purpose of this study was to investigate the effects of AVP with and without pre-treatment with the NO synthase inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME) on local brain tissue oxygenation in a beating heart model.Methods.Following approval of the Animal Investigational Committee, nine healthy piglets underwent general anaesthesia, and were instrumented with a probe in the cerebral cortex to measure PbtO2. Each animal was assigned to receive AVP (0.4?U?·?kg-1), and after a wash-out period, L-NAME (25?mg?·?kg-1 over 20?min) followed by AVP (0.4?U?·?kg-1). After each AVP administration, nitroglycerine (25?µg?·?kg-1 over 1?min) as a NO donor was infused to test the vascular reactivity independently from NOS inhibition.Findings.Three minutes after administration of AVP, PbtO2 increased significantly (P<.05; mean?±?SEM, 31?±?11 versus 43?±?14?mm?Hg, +39%), compared with baseline. After pre-treatment with L-NAME, the changes of PbtO2 after AVP were not significant (32?±?11 versus 28?±?10, -13%) when compared with the baseline.Conclusion.In this beating heart porcine model, local brain tissue oxygenation was improved after AVP alone, but not after inhibition of NO synthesis with L-NAME. [ABSTRACT FROM AUTHOR]

Arginine-vasopressin (AVP) can successfully stabilize hemodynamics in patients with advanced vasodilatory shock. It has been suggested that inhibition of cytokine-induced nitric oxide production may be an important mechanism underlying AVP-induced vasoconstriction. Therefore, serum concentrations of nitrite/nitrate (NOx), the stable metabolite of nitric oxide, were measured in patients suffering from advanced vasodilatory shock treated with either AVP in combination with norepinephrine (NE) or NE alone. This trial was a separate study arm of a previously published prospective, randomized, controlled study on the effects of AVP in advanced vasodilatory shock. Thirty-eight patients were prospectively randomized to receive a combined infusion of AVP (4 U h−1) and NE, or NE infusion alone. Serum NOx concentrations were measured at baseline, 24, and 48 h after randomization. The increase in mean arterial pressure during the first hour after study enrollment was documented in all patients. No difference in NOx concentrations was found between groups throughout the study period. AVP patients demonstrated a significantly greater increase in mean arterial pressure than NE patients (22 ± 10 vs. 5 ± 9 mmHg; P < 0.001). The magnitude of pressure response to AVP was not correlated with NOx concentrations before start of AVP infusion (Pearson's correlation coefficient, −.009; P = 0.971). Cardiovascular effects of AVP infusion in advanced vasodilatory shock are not mediated by a clinically relevant reduction in serum NOx concentrations. Therefore, hemodynamic improvement of patients in advanced vasodilatory shock during continuous infusion of AVP has to be attributed to other mechanisms than inhibition of nitric oxide synthase. In addition, the magnitude of pressure response to AVP is not correlated with baseline concentrations of NOx. [ABSTRACT FROM AUTHOR]

Background: Aim of this experimental animal study was to investigate the influence of vasopressin and amiodarone on cardiopulmonary resuscitation (CPR) outcome in a pig model of hypothermic cardiac arrest.Methods: After surface cooling to a core temperature of 26 degrees C, ventricular fibrillation was induced in 14 12-16-week-old domestic pigs. After 15 min of untreated cardiac arrest, a manual closed chest CPR was started and pigs were randomly assigned to two treatment groups: Group 1 pigs (n = 7) received vasopressin 0.4 U kg-1 as initial drug therapy, followed by a combination vasopressin (0.4 U kg-1) and amiodarone (4 mg kg-1) as subsequent drug therapy. Subsequent drug therapy was administered in animals without permanent restoration of spontaneous circulation after a first series of electrical countershocks 10 min after drug administration. Group 2 pigs (n = 7) received saline placebo as initial drug therapy and saline placebo and amiodarone (4 mg kg-1) as subsequent drug therapy.Results: Vasopressin significantly increased coronary perfusion pressure and defibrillation success (successful defibrillation in five of seven Group 1 vs. none of seven Group 2 pigs, P = 0.02). Due to refibrillation within 30-150 s, the 60-min survival rate was not improved by vasopressin. Subsequent drug therapy with amiodarone had no further effect on defibrillation success or the refibrillation rate.Conclusions: Data from this experimental animal model suggest that vasopressin and amiodarone may not be beneficial for treatment of ventricular fibrillation associated with severe hypothermia when concomitant measures at core rewarming are not applied. [ABSTRACT FROM AUTHOR]

The rationale for an arginine vasopressin (argipressin) infusion was put forward after it was discovered that patients in shock states might have an endogenous arginine vasopressin deficiency. Subsequently, several investigations impressively demonstrated that arginine vasopressin can successfully stabilise haemodynamics even in advanced vasodilatory shock. We report on physiological and pharmacological aspects of arginine vasopressin, and summarise current clinical knowledge on employing a continuous arginine vasopressin infusion in critically ill patients with catecholamine-resistant vasodilatory shock of different aetiologies. In view of presented experimental evidence and current clinical experience, a continuous arginine vasopressin infusion of ~2 to ~6 IU/h can be considered as a supplemental strategy to vasopressor catecholamines in order to preserve cardiocirculatory homeostasis in patients with advanced vasodilatory shock. Because data on adverse effects are still limited, arginine vasopressin should be reserved for patients in whom adequate haemodynamic stabilisation cannot be achieved with conventional vasopressor therapy or who have obvious adverse effects of catecholamines that result in further significant haemodynamic deterioration. For the same reasons, arginine vasopressin should not be used as a single, alternative vasopressor agent instead of catecholamine vasopressors. Future prospective studies will be necessary to define the exact role of arginine vasopressin in the therapy of vasodilatory shock. [ABSTRACT FROM AUTHOR]

Recent animal data have challenged the common clinical practice to avoid vasopressor drugs during hypothermic cardiopulmonary resuscitation (CPR) when core temperature is below 30 degrees C. In this report, we describe the case of a 19-year-old-female patient with prolonged, hypothermic, out-of-hospital cardiopulmonary arrest after near drowning (core temperature, 27 degrees C) in whom cardiocirculatory arrest persisted despite 2 mg of intravenous epinephrine; but, immediate return of spontaneous circulation occurred after a single dose (40 IU) of intravenous vasopressin. The patient was subsequently admitted to a hospital with stable haemodynamics, and was successfully rewarmed with convective rewarming, but died of multiorgan failure 15 h later. To the best of our knowledge, this is the first report about the use of vasopressin during hypothermic CPR in humans. This case report adds to the growing evidence that vasopressors may be useful to restore spontaneous circulation in hypothermic cardiac arrest patients prior to rewarming, thus avoiding prolonged mechanical CPR efforts, or usage of extracorporeal circulation. It may also support previous experience that the combination of both epinephrine and vasopressin may be necessary to achieve the vasopressor response needed for restoration of spontaneous circulation, especially after asphyxial cardiac arrest or during prolonged CPR efforts. [ABSTRACT FROM AUTHOR]