Human superoxide dismutase failed to limit the size of myocardial infarct after 20-, 30-, or 60-minute ischemia and 72-hour reperfusion in the rabbit.

The effect of superoxide dismutase (SOD) on the size of the myocardial infarct resulting from various durations of ischemia and a 72-hour reperfusion was examined in the rabbit. A coronary branch of the circumflex artery was occluded for 20, 30, or 60 min and then reperfused. Seventy-two hours after the coronary occlusion, the infarct size and the size of the area at risk (vascular bed of occluded coronary artery) were determined by histology (hematoxylin-eosin and Mallory's staining) and by fluorescent particles, respectively. Human SOD (45,000 units/kg) was injected intravenously as a bolus in SOD-treated rabbits, while only saline was administered to control rabbits. The percentage of the area at risk which actually infarcted (%I/AAR) was 25.5 +/- 12.9% (mean +/- S.D.) in the 20-min ischemia control group (n = 9), 19.7 +/- 10.2% in the 20-min ischemia SOD group (n = 9), 44.8 +/- 9.0% in the 30-min ischemia control group (n = 9), 41.0 +/- 6.3% in the 30-min ischemia SOD group (n = 9), 74.2 +/- 13.8% in the 60-min ischemia control group (n = 9), and 76.6 +/- 8.2% in the 60-min ischemia SOD group (n = 7). The %I/AAR was not significantly different between the control and SOD groups for any duration of ischemia. Heart rate, blood pressure, and the size of area at risk were comparable in all six groups. These findings suggested that oxygen-free radicals produced during initial moments of reperfusion were unlikely to contribute to myocardial necrosis regardless of the duration of ischemia in the rabbit.