DIRECT-CURRENT SHOCKS TO THE HEART GENERATE FREE-RADICALS - AN ELECTRON-PARAMAGNETIC-RESONANCE STUDY

Objectives. We sought to demonstrate that direct current (DC) shocks t o the heart generate free radicals. Background. Although it is a lifes aving maneuver, defibrillation is known to have myocardial toxicity. T he mechanism of this toxicity is unknown. If DC shocks generate free r adicals, free radicals could be a mechanism of myocardial injury. Meth ods. In a canine model, DC shocks of 10 to 100 J were delivered to the epicardium of both beating and fibrillating hearts, and 200-J transth oracic shocks were administered in dogs with beating hearts. Ascorbate free radical (AFR) concentration was measured in arterial blood and b lood continuously withdrawn from the coronary sinus. In some dogs, the antioxidant enzymes superoxide dismutase (15,000 U/kg) and catalase ( 55,000 U/kg) (SOD/Cat) were administered before shocks. Results. Ascor bate free radicals were generated by DC shocks. A peak AFR increase of 14 +/- 2% (mean +/- SEM) was seen 5 to 6 min after 100-J epicardial s hocks. A peak AFR increase of 7 +/- 5% occurred after transthoracic sh ocks. There was a significant linear relation between the shock energy and peak percent AFR increase: %AFR increase = 0.18 (Shock energy) 2.9 (r = 0.73, p < 0.0001). Shocks delivered to hearts in ventricular fibrillation (30 s) resulted in generation of AFR equal to but not gre ater than that observed during similar shocks delivered to beating hea rts in sinus rhythm. Multiple successive shocks (100 J delivered twice or five times) did not result in a greater AFR increase than single 1 00-J shocks, indicating that peak, not cumulative, energy is the princ ipal determinant of AFR increase. Animals receiving SOD/Cat before sho ck administration showed significant attenuation of the AFR increase. Conclusions. Direct current epicardial and transthoracic shocks genera te free radicals; antioxidant enzymes reduce the free radical generati on by shocks.