Study objectives: 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.
Design: 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
Measurements and results: 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).
Conclusions: Captopril lowers coronary venous AFR
concentration after high-energy epicardial shocks.