Captopril Lowers Coronary Venous Free Radical Concentration After Direct Current Cardiac Shocks

Abstract

Direct current (DC) shocks to the heart cause morphologic and functional myocardial damage. Previous studies have suggested that acute DC shock injury is free radical mediated and that the administration of antioxidant enzymes superoxide dismutase and catalase can reduce the level of DC shock-induced free radicals. Angiotensin-converting enzyme (ACE) inhibitors are clinically used drugs that may scavenge free radicals or reduce free radical generation. The objective of our study was to determine whether the ACE inhibitor captopril lowers free radicals after DC shocks. In six open-chest dogs, we administered 100-J DC shocks to the epicardium, before and after administration of captopril, 3 mg/kg. We used electron paramagnetic resonance measurements of arterial and coronary venous ascorbate free radical (AFR) as a real-time marker of free radical generation (total oxidative flux). Captopril resulted in a significant lowering of coronary venous AFR concentration: the peak rise in AFR after 100-J shocks was 17.3+/-3.4% (mean +/- SEM before captopril vs. 3.2+/-4.0% after captopril; p<0.05). Captopril lowers coronary venous AFR concentration after high-energy epicardial shocks.