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Ann Thorac Surg 1991;52:918-926
© 1991 The Society of Thoracic Surgeons
a Departments of Surgery, University of Connecticut School of Medicine, Farmington, Connecticut USA
b The Baystate Medical Center, Springfield, Massachusetts USA
* Address reprint requests to Dr Engelman, Baystate Medical Center, 759 Chestnut St, Springfield, MA 01107.
Captopril is an angiotensin-converting enzyme inhibitor that has been reported to be effective in salvaging postischemic reperfused myocardium by its ability to function as a free radical-scavenging agent. A study was performed in the isolated porcine-heart model evaluating the influence of pretreatment with captopril on salvage of myocardium after an induced myocardial infarction. Measurement was carried out of regional and global myocardial function, myocardial high-energy phosphate levels, creatine kinase release, malonaldehyde formation, and 6-keto-prostaglandin F1α generation. In an in vitro preparation, the influence of captopril for scavenging various free radicals was evaluated. A dose-response curve was carried out using this free radical-generating system and differing levels of captopril. Results of the study demonstrate that pretreatment with captopril at a 45-µmol/L level reduced reperfusion injury in the pig heart model. This was manifested by improved cardiac performance, a reduction in creatine kinase release, and reduced malonaldehyde generation. In vitro evaluation of captopril and its free radical-scavenging ability indicated that it is a weak scavenger of superoxide anions (O2 –) but behaves as a potent scavenger of hydroxyl radicals (–OH) as well as hypohalite radicals (OCl–). Based on the influence of captopril in reducing lipid peroxidation (decreased malonaldehyde formation) and its documented ability to scavenge –OH as well as OCl–, it is suggested that myocardial preservation in a postinfarction model is due primarily to its free radicalscavenging activity, primarily of the potent free radicals –OH and OCl–.
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