Abstract
Ischemia-reperfusion injury is caused by reactive oxygen production after revascularization. It is characterized by elevated ST segments on electrocardiogram (ECG), although the mechanisms remain unknown. In the present study, we reproduced the ST segment changes observed during ischemia-reperfusion injury by exposing bullfrog hearts to hydrogen peroxide (H(2)O(2)). The ECG showed a marked elevation of the ST segments, and the action potential in cardiomyocytes demonstrated shortening of its duration. H(2)O(2) exposure did not affect the abundance of K(ATP) channel proteins. However, pharmacological blockade by glibenclamide significantly suppressed H(2)O(2)-induced changes in ECG and tended to suppress cardiac action potentials. K(ATP) channel stimulation by H(2)O(2) is thought to be responsible for generating an electrical difference in cardiomyocytes and the subsequent ST segment elevation.