CAPTOPRIL DECREASES STRESS ULCERATION WITHOUT AFFECTING GASTRIC PERFUSION DURING CANINE HEMORRHAGIC-SHOCK

The renin-angiotensin axis has recently been called the source of disp roportionate splanchnic vasoconstriction during shock, and blocking th is axis decreased gastric stress ulceration during swine cardiogenic s hock. The present study tested whether the angiotensin converting enzy me inhibitor captopril would prevent stress ulceration when given afte r the onset of canine hemorrhagic shock, and whether any detrimental e ffects would result from enhancing splanchnic perfusion with captopril during hemorrhagic shock. We found that captopril treatment was assoc iated with a decrease in gastric mucosal injury and with a marked decr ease in systemic acidosis. Captopril enhanced blood flow to the small intestine, pancreas, liver, and spleen, but not flow to the stomach, d uring shock. Following the reinfusion of shed blood, the captopril-tre ated animals had decreased mean blood pressures and increased heart ra tes compared with untreated animals. We found captopril alleviated the stress ulceration produced by canine hemorrhagic shock, but concluded that the likely mechanism was alleviating systemic acidosis through e nhanced perfusion of other viscera rather than a specific enhancement of gastric perfusion.