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

Abstract

Hypercapnia (HC) improves systemic oxygen delivery (DO 2 ) and microvascular hemoglobin oxygenation of the mucosa (mHbO 2 ). 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 mg/kg) on hemodynamic variables and mHbO 2 during normocapnia or HC (end-tidal CO 2 70 mmHg). In a control group, animals were subjected to HC alone. mHbO 2 was measured by reflectance spectrophotometry, systemic DO 2 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, DO 2 increased from 12G1 to 16G1 ml/kg per min and mHbO 2 from 70G4 to 80G2%. By contrast, additional vasopressin V 1A receptor blockade abolished the increase in mHbO 2 (80G2 vs 69G2%) without altering the increase in DO 2 (16G1 vs 19G 2 ml/kg per min). Vasopressin V 1A receptor blockade (VB) during normocapnia neither affected DO 2 (13G1 vs 14G1 ml/kg per min) nor mHbO 2 (75G3 vs 71G5%). Vasopressin V 1A receptor blockade abolished the increase in mHbO 2 during HC independent of DO 2 . 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.

Exogenous vasopressin dose-dependently modulates gastric microcirculatory oxygenation in dogs via V1A receptor

“…So far, attempts to specifically resuscitate the gut have shown to be unsuccessful [10]. In previous studies, we could show that hypercapnia increased gastric μHbO 2 in anesthetized dogs [11] and preserved intestinal μHbO 2 in septic rats [12]. Both effects were abolished during V1A receptor blockade indicating an involvement of the vasopressin system.…”

Effets des vasoconstricteurs sur la microcirculation

“…Enfin, l'augmentation de la DO 2 systémique et de l'oxygé-nation de la microcirculation splanchnique (muqueuse gastrique), en réponse à l'induction d'une hypercapnie, est médiée par le récepteur V1A de la vasopressine chez le chien sain [54].…”

Hypercapnia counteracts captopril-induced depression of gastric mucosal oxygenation

“…Experiments were performed with the approval of the Local Animal Care and Use Committee (North RhineWestphalia State Agency for Nature, Environment and Consumer Protection,Recklinghausen,Germany;. The same group of five dogs used in this study was used in another study published previously (Vollmer et al 2013). Each dog underwent each protocol in a randomized order and served as its own control.…”

“…After pretreatment, HC was maintained for an additional hour. The results of this control group have been published already as those of the control group (Vollmer et al 2013) because we are forced by law to minimize animal experiments. However, this group was randomized in this series.…”

“…Additionally, it protects microvascular oxygenation of the gastric mucosa during physiological conditions (Schwartges et al 2008) and hemorrhagic shock (Schwartges et al 2010). In this context, we have recently shown that the increase in gastric mucosal oxygenation during otherwise physiological conditions is mediated via vasopressin V1A receptors (Vollmer et al 2013) and might be due to increased levels of vasopressin during HC (Philbin et al 1970). However, HC interacts with other hormone systems as well.…”