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

Hypercapnia (HC) improves systemic oxygen delivery (DO2) and microvascular hemoglobin oxygenation of the mucosa (mu HbO2). 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 V-1A receptor blockade ([Pmp(1), Tyr(Me)(2)]-Arg(8)-Vasopressin, 35 mu g/kg) on hemodynamic variables and mu HbO(2) during normocapnia or HC (end-tidal CO2 70 mmHg). In a control group, animals were subjected to HC alone. mHbO(2) 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 meanGS. E. M. for nZ5 animals. During HC alone, DO2 increased from 12 +/- 1 to 16 +/- 1 ml/kg per min and mHbO(2) from 70 +/- 4 to 80 +/- 2%. By contrast, additional vasopressin V-1A receptor blockade abolished the increase in mu HbO(2) (80 +/- 2 vs 69 +/- 2%) without altering the increase in DO2 (16 +/- 1 vs 19 +/- 2 ml/kg per min). Vasopressin V-1A receptor blockade (VB) during normocapnia neither affected DO2 (13 +/- 1 vs 14 +/- 1 ml/kg per min) nor mHbO(2) (75 +/- 3 vs 71 +/- 5%). Vasopressin V-1A receptor blockade abolished the increase in mHbO(2) during HC independent of DO2. Thus, in contrast to its generally vasoconstrictive properties, the vasopressin V-1A receptors seem to mediate the increase in gastric microcirculatory mucosal oxygenation induced by acute HC.