Hypercapnia (HC) increases systemic oxygen delivery (DO 2 ) and gastric mucosal oxygenation. However, it activates the renin-angiotensin-aldosterone system (RAAS), which conversely reduces mesenteric perfusion. The aims of this study were to evaluate the effect of RAAS inhibition during normocapnia and HC on oral and gastric mucosal oxygenation (mHbO 2 ) and to assess the effect of blood pressure under these circumstances. Five dogs were repeatedly anesthetized to study the effects of ACE inhibition (ACE-I; 5 mg/kg captopril, followed by 0.25 mg/kg per h) on mHbO 2 (reflectance spectrophotometry) and hemodynamic variables during normocapnia (end-tidal CO 2 Z35 mmHg) and HC (end-expiratory carbon dioxide (etCO 2 )Z70 mmHg). In the control group, the dogs were subjected to HC alone. To exclude the effects of reduced blood pressure, in one group, blood pressure was maintained at baseline values via titrated phenylephrine (PHE) infusion during HC and additional captopril infusion. ACE-I strongly reduced gastric mHbO 2 from 72G2 to 65G2% and mean arterial pressure (MAP) from 64G2 to 48G4 mmHg, while DO 2 remained unchanged. This effect was counteracted in the presence of HC, which increased gastric mHbO 2 from 73G3 to 79G6% and DO 2 from 15G2 to 22G4 ml/kg per min during ACE-I without differences during HC alone. However, MAP decreased similar to that observed during ACE-I alone from 66G3 to 47G5 mmHg, while left ventricular contractility (dP max ) increased from 492G63 to 758G119 mmHg/s. Titrated infusion of PHE had no additional effects on mHbO 2 . In summary, our data suggest that RAAS inhibition reduces gastric mucosal oxygenation in healthy dogs. HC not only abolishes this effect, but also increases mHbO 2 , DO 2 , and dP max . The increase in mHbO 2 during ACE-I under HC is in accordance with our results independent of blood pressure.

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