The role of angiotensin in the pathophysiology of mesenteric vasospasm raises the question whether angiotensin-converting enzyme (ACE) inhibitors can influence the sequelae of shock on the mesenteric circulation. The purpose of this study was to investigate the effect of captopril on the metabolic consequences of the nonocclusive mesenteric infarct. Thirty pigs were used. The cardiogenic shock was induced by an infusion of 10% hydroxyethyl starch into the pericardium over 10 min. In all groups, except the control group, the ACE inhibitor captopril was given as a bolus of 0.25 mg/kg and then 10 mg/kg/min continuously up to a total of 50 mg. The positive effect of captopril on the mesenteric circulation was verified by a significantly smaller increase of lactate, lesser pH decrease in the superior mesenteric vein. The shock-induced acidosis in the mesenteric circulation was less profound in therapy groups as compared with the control group. Systemic therapy with ACE inhibitor is more effective than local application. The effect of captopril treatment inherently relies on the timing of initiation.