Abstract
Summary
Anesthetized cats subjected to hemorrhage were treated with captopril, a CEI (0.5 μg/kg/hr) alone or in conjunction with angiotensin II (10 μg/kg/hr). Angioten-sin II administration significantly reduced survival time (110 vs 64 min) and lowered superior mesenteric artery flow (SMAF) immediately after reinfusion (8.5 vs 2.2 ml/kg/ min). These results suggest that blockade of angiotensin II formation is a prominent aspect of the beneficial actions of captopril in hemorrhage. Furthermore, captopril potentiated the vascular effects of bradykinin at normal blood pressures but not in hemor-rhagic hypotension. In the same experiments, captopril blocked the vascular effects of angiotensin I at both pressures. Thus, bradykinin potentiation is not essential for the beneficial actions of captopril in hemorrhagic shock, since hypotension abolishes the bra-dykinin-potentiating effects of captopril. Reduction of angiotensin II formation appears to be a major mechanism of captopril action in prolonging survival after hemorrhage.
We wish to thank Dr. Michael Antonaccio of the Squibb Institute for Medical Research, Princeton, New Jersey 08540 for the generous supply of SQ-14,225 (Captopril®, Squibb).
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