The role of oxygen free radicals (OFR) generated early during myocardial reperfusion in the genesis of myocardial necrosis was studied in 26 pigs submitted to transient coronary occlusion followed by one of three different reperfusion protocols. In group A, a selective intracoronary infusion of a Ringer solution was started after 60 min of coronary occlusion, and reperfusion was performed 4 min later. The infusion was maintained during the first 6 min of reperfusion at a rate of 3 ml/min. In group B, the Ringer solution administered during reperfusion contained a high concentration (2.778 U/ml) of superoxide dismutase (SOD). In group C, reperfusion was performed after 60 min of coronary occlusion with no intracoronary infusion. Twenty-four hours later the heart was excised and the area at risk and infarct size were measured by in vivo fluorescein injection and triphenyl-tetrazolium chloride staining respectively. The area at risk was similar in the 3 groups: 15.03 +/- 2.6%, 13.26 +/- 3.3% and 16.34 +/- 6.7% of ventricular mass in groups A, B, and C, respectively (p = 0.42). No differences between groups were observed in infarct size, either when measured as a percent of ventricular mass (10.04 +/- 3.8%, 9.31 +/- 3.8% and 10.1 +/- 2.4% in groups A, B, and C, p = 0.91) or as a percent of the area at risk (64.63 +/- 18.5%, 67.81 +/- 16.1%, and 61.35 +/- 6.7%, respectively, p = 0.72). Thus, the intracoronary administration of SOD during the early reperfusion has not beneficial effect on infarct size. This results suggest that the early burst of OFR is not a major determinant of infarct size in the pig.