O2-radical scavengers and allopurinol prevented the reduction of sarcolemmal Na+-K+-ATPase activity caused by ischemia and reperfusion in isolated guinea pig hearts.
The role of O2 free radicals in the reduction of sarcolemmal Na+-K+-ATPase, which occurs during reperfusion of ischemic heart, was examined in isolated guinea pig heart using exogenous scavengers of O2 radicals and an inhibitor of xanthine oxidase. Ischemia and reperfusion reduced Na+-K+-ATPase activity and specific 3Houabain binding to the enzyme in ventricular muscle homogenates and also markedly lowered sodium pump activity estimated from ouabain-sensitive 86Rb+ uptake by ventricular muscle slices. These effects of ischemia and reperfusion were prevented to various degrees by O2-radical scavengers, such as superoxide dismutase, catalase, dimethyl-sulfoxide, histidine, or vitamin E or by the xanthine oxidase inhibitor, allopurinol. The degree of protection afforded by these agents paralleled that of reduction in enhanced lipid peroxidation of myocardial tissue as estimated from malondialdehyde production. These results strongly suggest that O2 radicals play a crucial role in the injury to sarcolemmal Na+-K+-ATPase during reperfusion of ischemic heart.
Kim et al. (Sun,) conducted a other in Ischemia-reperfusion injury. O2-radical scavengers or allopurinol vs. Ischemia and reperfusion without scavengers/inhibitors was evaluated on Na+-K+-ATPase activity, specific [3H]ouabain binding, and sodium pump activity. O2-radical scavengers and allopurinol prevented the reduction of sarcolemmal Na+-K+-ATPase activity caused by ischemia and reperfusion in isolated guinea pig hearts.