Responses to Nitroprusside Following Hemorrhage in Anesthetized Pigs
Summary rept. 1987-1989,
LETTERMAN ARMY INST OF RESEARCH PRESIDIO OF SAN FRANCISCO CA
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The present study was undertaken to examine the physiologic and metabolic effects of pharmacologic vasodilation on recovery from non-lethal severe hemorrhage. It was hypothesized that following hemorrhage a reduction in aortic hydrostatic afterload would lead to a beneficial rise in cardiac output, which would, in turn, improve oxygen delivery. In this study, pigs n6 control and n7 experimental of body weight 23.5 kg were subjected to a 40, 28 mlkg, arterial hemorrhage while under chloralose-urethane anesthesia. The subjects in the experimental group were then administered nitroprusside at a dose sufficient to maintain mean arterial blood pressure at 50 mm Hg for 60 minutes. Nitroprusside-induced vasodilation significantly lowered systemic vascular resistance, but produced no significant change in the pulmonary vascular bed. Nitroprusside did not produce a significant effect on cardiac output, but did lower oxygen delivery per unit weight. Thus, the proposed enhancement of tissue oxygenation resulting from a lowered myocardial afterload did not occur. Venodilation, as a result of nitroprusside administration, may have lowered venous return to the heart and thus blunted the expected rise in cardiac output. As a result of this study, we believe that aggressive vasodilator therapy is an inappropriate treatment following significant systemic hemorrhage.