Vasopressin V1A receptors mediate the increase in gastric mucosal oxygenation during hypercapnia

Abstract

Hypercapnia (HC) improves systemic oxygen delivery (DO2) and microvascular hemoglobin oxygenation of the mucosa (μHbO2). Simultaneously, HC increases plasma levels of vasopressin. Although vasopressin is generally regarded a potent vasoconstrictor particularly in the splanchnic region, its effects on splanchnic microcirculation during HC is unclear. The aim of this study was to evaluate the role of endogenous vasopressin on gastric mucosal oxygenation and hemodynamic variables during physiological (normocapnia) and hypercapnic conditions. Five dogs were repeatedly anesthetized to study the effect of vasopressin V1A receptor blockade ([Pmp1,Tyr(Me)2]-Arg8-Vasopressin, 35 μg/kg) on hemodynamic variables and μHbO2 during normocapnia or HC (end-tidal CO2 70 mmHg). In a control group, animals were subjected to HC alone. μHbO2 was measured by reflectance spectrophotometry, systemic DO2 was calculated from intermittent blood gas analysis, and cardiac output was measured by transpulmonary thermodilution. Data are presented as mean±s.e.m. for n=5 animals. During HC alone, DO2 increased from 12±1 to 16±1 ml/kg per min and μHbO2 from 70±4 to 80±2%. By contrast, additional vasopressin V1A receptor blockade abolished the increase in μHbO2 (80±2 vs 69±2%) without altering the increase in DO2 (16±1 vs 19±2 ml/kg per min). Vasopressin V1A receptor blockade (VB) during normocapnia neither affected DO2 (13±1 vs 14±1 ml/kg per min) nor μHbO2 (75±3 vs 71±5%). Vasopressin V1A receptor blockade abolished the increase in μHbO2 during HC independent of DO2. Thus, in contrast to its generally vasoconstrictive properties, the vasopressin V1A receptors seem to mediate the increase in gastric microcirculatory mucosal oxygenation induced by acute HC.