Reactive oxygen species (ROS) are formed at an accelerated rate in postisch
emic myocardium. Cardiac myocytes, endothelial cells, and infiltrating neut
rophils contribute to this ROS production. Exposure of these cellular compo
nents of the myocardium to exogenous ROS can lead to cellular dysfunction a
nd necrosis. While it remains uncertain whether ROS contribute to the patho
genesis of myocardial infarction, there is strong support for ROS as mediat
ors of the reversible ventricular dysfunction (stunning) that often accompa
nies reperfusion of the ischemic myocardium. The therapeutic potential of f
ree radical-directed drugs in cardiac disease has not been fully realized.
Am J Med. 2000;109:315-323. (C) 2000 by Excerpta Medica, Inc.