Jj. Cullen et al., CAPTOPRIL DECREASES STRESS ULCERATION WITHOUT AFFECTING GASTRIC PERFUSION DURING CANINE HEMORRHAGIC-SHOCK, The journal of trauma, injury, infection, and critical care, 37(1), 1994, pp. 43-49
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.