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Oxidative stress and cardiac disease

Authors
Journal
The American Journal of Medicine
0002-9343
Publisher
Elsevier
Publication Date
Volume
109
Issue
4
Identifiers
DOI: 10.1016/s0002-9343(00)00467-8
Keywords
  • Physiology In Medicine
Disciplines
  • Medicine

Abstract

Abstract Reactive oxygen species (ROS) are formed at an accelerated rate in postischemic myocardium. Cardiac myocytes, endothelial cells, and infiltrating neutrophils contribute to this ROS production. Exposure of these cellular components of the myocardium to exogenous ROS can lead to cellular dysfunction and necrosis. While it remains uncertain whether ROS contribute to the pathogenesis of myocardial infarction, there is strong support for ROS as mediators of the reversible ventricular dysfunction (stunning) that often accompanies reperfusion of the ischemic myocardium. The therapeutic potential of free radical-directed drugs in cardiac disease has not been fully realized.

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