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 ODFR scavengers on ischemia-induced dysfunction of cardiac sympathetic nerves. Mongrel dogs were anesthetized and instrumented for recording heart rate, arterial pressure, systolic wall thickening, and left anterior descending coronary artery (LAD) and left circumflex coronary artery (LCX) flow velocities. Bilateral stellate stimulation was performed, measuring changes in an index of coronary vascular resistance (% delta CVR) before and after 15 min of LAD occlusion. Superoxide dismutase (SOD) and catalase (CAT) were infused intravenously for 30 min beginning 10 min before occlusion. With vehicle (n = 13), % delta CVR was significantly 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 SOD and CAT were infused (n = 10; for LAD, 39 +/- 5 to 41 +/- 5%; for LCX, 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 function (percent of baseline) was greater in SOD and CAT after reperfusion (26 +/- 16% vs. -30 +/- 11% at 90 min of reperfusion, P < 0.05). We conclude that ODFR contribute not only to myocardial stunning but also to neural stunning of sympathetic cardiac innervation after brief ischemia.