Captopril lowers coronary venous free radical concentration after direct current cardiac shocks

Study objectives: Direct current (DC) shocks to the heart cause morphologic and functional myocardial damage, Previous studies have suggested that acu te 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-concerting enzyme (ACE) inhi bitors are clinically used drugs that may scavenge free radicals or reduce free radical generation. The objective of our study was to determine whethe r the ACE inhibitor captopril lowers free radicals after DC shocks. Design: In six open-chest dogs, we administered 100-J DC shocks to the epic ardium, before and after administration of captopril, 3 mg/kg, We used elec tron paramagnetic resonance measurements of arterial and coronary venous as corbate free radical (AFR) as a real-time marker of free radical generation (total oxidative flux). Measurements and results: Captopril resulted in a significant lowering of c oronary venous AFR concentration: the peak rise in AFR after 100-J shocks w as 17.3 +/- 3.4% (mean a SEM before captopril vs 3.2 +/- 4.0% after captopr il; p < 0.05), Conclusions: Captopril lowers coronary venous AFR concentration after high- energy epicardial shocks.