Superoxide dismutase enhances recovery following myocardial ischemia

Abstract

Oxygen-derived free radicals, specifically superoxide (O2-) and the hydroxyl radical (OH .cntdot.), were implicated as possible mediators in the development of myocardial damage induced by ischemia and reflow. The ability of superoxide dismutase (SOD), a O2- scavenging enzyme, to protect the heart against functional and structural alterations due to ischemia and reflow was examined. An isolated perfused rabbit interventricular septal preparation was used for these experiments. Septa were treated with SOD by adding either 10 or 20 .mu.g/ml of the enzyme to the perfusion solution 15 min prior to ischemia and during reflow. Other septa were not treated. Septa were made ischemic for 1 h and reperfused for 1 h. The contractile performance of reperfused septa was found to be significantly improved in SOD-treated septa when compared with nontreated septa. After 60 min of reflow, values for nontreated, 10 and 20 .mu.g/ml SOD-treated septa, respectively, were 48.5 .+-. 5.2 (SE), 67.4 .+-. 4.2, and 82.0 .+-. 3.8% of control values for developed tension. The rise in resting tension observed with reflow was significantly decreased. SOD treatment also provided significant protection of myocardial ultrastructure. The percent of myocytes showing normal structure was increased .apprx. 40%, and the percentages of myocytes showing mild or severe damage were decreased .apprx. 30 and 15%, respectively, for SOD-treated septa. Vessel structure showed a similar trend. SOD preserves myocardial function and structure in septa reperfused following ischemia. Oxygen-derived free radicals may be involved in the damage resulting from ischemia and reflow.