OXYGEN-DERIVED FREE-RADICALS CONTRIBUTE TO NEURAL STUNNING IN THE CANINE HEART

Oxygen-derived free radicals (ODFR) contribute to delayed recovery of myocardial function after brief ischemia. We examined the effect of OD FR scavengers on ischemia-induced dysfunction of cardiac sympathetic n erves. Mongrel dogs were anesthetized and instrumented for recording h eart rate, arterial pressure, systolic wall thickening, and left anter ior descending coronary artery (LAD) and left circumflex coronary arte ry (LCX) flow velocities. Bilateral stellate stimulation was performed , measuring changes in an index of coronary vascular resistance (%Delt a CVR) before and after 15 min of LAD occlusion. Superoxide dismutase (SOD) and catalase (CAT) were infused intravenously for 30 min beginni ng 10 min before occlusion. With vehicle (n = 13), %Delta CVR was sign ificantly attenuated in LAD after ischemia and 30-min reperfusion [39 +/- 3 to 13 +/- 2%, P < 0.05; for LCX, 42 +/- 4 to 45 +/- 7%, P = not significant (NS)]; however, no attenuation was seen in dogs in which S OD and CAT were infused (n = 10; for LAD, 39 +/- 5 to 41 +/- 5%; for L CX, 46 +/- 7 to 47 +/- 6%; P = NS). Baseline and stimulated changes in hemodynamics were similar between groups. The %Delta CVR in the LCX ( control) bed was not affected by SOD and CAT. Recovery of myocardial f unction !percent of baseline) was greater in SOD and CAT after reperfu sion (26 +/- 16% vs. -30 +/- 11% at 90 min of reperfusion, P < 0.05). We conclude that ODFR contribute not only to myocardial stunning but a lso to neural stunning of sympathetic cardiac innervation after briefi schemia.