Effect of intracoronary superoxide dismutase on regional function in stunned myocardium.

This study investigates the ischemic-time dependency of dysfunction in reversibly ischemic myocardium and the effect of postischemic oxygen free radical scavenging thereupon. In open chest pigs, occlusion of the distal left anterior descending coronary artery (LAD) for 4 (n = 5), 8 (n = 5), or 12 min (n = 5) resulted in paradoxical systolic and diastolic regional function, measured by ultrasonic crystals. With onset of reperfusion, systolic shortening (SS) and diastolic lengthening (DL) normalized completely in the 4- and 8-min groups, followed by a significant decrease to 50% control in the 8-min group. In the 12-min group, recovery of SS and DL was only partial. In two further groups, animals received an intracoronary infusion of either recombinant human superoxide dismutase (SOD, n = 6) or placebo (n = 6), starting with reperfusion after an 8-min LAD occlusion. SOD improved recovery of SS compared with placebo (p less than 0.05), but DL and the depression of SS during later reperfusion were not influenced. Mitochondrial function after 90 min of reperfusion was not impaired in ischemic-reperfused compared to control myocardium. We conclude that the degree of postischemic dysfunction increases with the duration of ischemia. Oxygen free radical scavenging by SOD, starting not before reperfusion, fails to prevent myocardial stunning. Mitochondrial function is intact in such myocardium.