[An in vitro study of the mechanism by which captopril attenuates myocardial reperfusion damage] (original) (raw)
Archivos del Instituto de CardiologĂa de MĂ©xico
Abstract
The purpose of this study was to establish the molecular mechanism whereby captopril prevents the formation of active oxygen species, since many studies have provided evidence that postischemic myocardial dysfunction is mediated, at least in part, by the generation of these agents. Results indicate that captopril is a potent inhibitor of certain reactions mediated by O2-. However, this interference of captopril was not understood as an scavenging activity against the free radicals generated. The data could be explained by considering a direct interaction of captopril with the metal ions present that catalyse the formation of O2-. This mechanism could be of biological relevance.
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