To evaluvate the hypothesis that reperfusion injury and reperfusion arrhythmia could be caused by oxyzen free redicals and that prolonged myocardial dysfunction could be induced by oxyzen free redical.

Experimnetal model of anesthetized open chest dogs was used. Coronary artery was occluded for 60 minutes and reperfusion was performed 4 hours. In 5 dogs, superoxide dismutase and catalase were infused concomitantly 15 minutes after coronary occlusion to 15 minutes after reperfusion. In 9 dogs, 0.9% saline was infused instead of free redical scavengers. Hemodynamic parameters such as heart rate, left ventricular peak systolic pressure, end-diastolic pressure, peak positive dP/dt, and peak negative dP/dt were analysed. Infarct size was estimated by the unstained area in nitroblue tetrazolium staining and risk area was calculated from the unstained area after methylen blue infusion. Regional systolic function was observed in systolic thickening of ischemic area by echocardiogram.

1) Reperfusion arrhythmia occurred in 67% of control group and in 50% of drug treated group.

2) Systolic hemodynamic parameters such as peak systolic pressure, peak positive dP/dt showed no difference between control and drug-treated group.

3) Diastolic parameters such as end-diastolic pressure and peak negative dP/dt were not different in two groups.

4) Regional systolic parameter measured by systolic thickening in ischemic area improved after reperfusion and continued to be better in drug treated group than in control group.

5) Infarct size, risk area, ratio of infarct size to risk aera were not different in two groups.

Superoxide dismutase and catalase showed no effect in reducing the infarct size in anesthetized open chest canine model with 60 minutes of coronary occlusion 4 hours of reperfusion. However, postischemic prolonged myocardial dysfunction tended of improve-after reperfusion in drug treated group.