The effects of an intracoronary infusion of superoxide dismutase on infarct size were studied in 16 pigs submitted to a 48-min coronary occlusion of the mid left anterior descending coronary artery followed by reperfusion for 24 h. Areas at risk marked with fluorescein and infarct sizes calculated with triphenyl tetrazolium chloride staining 24 h after the occlusion were similar in the five control animals with coronary reperfusion alone, in the five animals with an intracoronary infusion of lactate Ringer initiated 3 min before reperfusion and maintained for 33 min and in the six animals with superoxide dismutase added to the solution of lactate Ringer and infused at a rate of 2500 units/min. The ratios infarct size/area at risk were respectively 0.50 +/- 0.10, 0.65 +/- 0.04 in the three study groups (NS). The extent of intramyocardial hemorrhage, evaluated by morphometric analysis was also similar 0.90 +/- 0.29 x 10(6), 0.70 +/- 0.14 and 1.62 +/- 0.42 red blood cells/mm3 of tissue (NS). The superoxide dismutase infusion, however, resulted in significantly fewer early reperfusion arrhythmias which involved 23 +/- 15 s of each minute electrocardiographic recording in the superoxide dismutase group, compared to 37 +/- 13 s in the lactate Ringer group and 45 +/- 14 s in the control group (p = 0.004). The lack of an effect of intracoronary infusion of superoxide dismutase on infarct size suggests that in this experimental model, extracellular superoxide radicals generated during early reperfusion have no major role on myocardial cell necrosis and microvascular damage. Reperfusion arrhythmias were, however, reduced.