[An in vitro study of the mechanism by which captopril attenuates myocardial reperfusion damage].
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.
Jay
D
D
Departamento de Bioquímica, Instituto Nacional de Cardiología Ignacio Chávez.
Zamorano
R
R
Cuéllar
A
A
Muñoz
E
E
Gleason
R
R
D000818:Animals; D002216:Captopril / Q000494:pharmacology / Q000627:therapeutic use*; D004353:Drug Evaluation, Preclinical; D004347:Drug Interactions; D004837:Epinephrine / Q000378:metabolism; D005609:Free Radicals; D066298:In Vitro Techniques; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism; D010084:Oxidation-Reduction / Q000187:drug effects; D010659:Phenylhydrazines / Q000378:metabolism; D013778:Tetrazolium Salts / Q000378:metabolism
D005609:Free Radicals; D010659:Phenylhydrazines; D013778:Tetrazolium Salts; C042207:4-anisyltetrazolium blue; C030299:phenylhydrazine; D002216:Captopril; D004837:Epinephrine
Estudio in vitro del mecanismo por el cual el captopril atenúa el daño miocárdico por reperfusión.