title: Oxidative stress and cardiac disease.
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.
authors.affiliation: Department of Molecular and Cellular Physiology, Louisiana State University Health Sciences Center, 1501 Kings Highway, Shreveport, Louisiana, USA.
authors.forename: D J
authors.initials: DJ
authors.lastname: Lefer
authors.forename: D N
authors.initials: DN
authors.lastname: Granger
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D002320:Cardiovascular Physiological Phenomena; D003327:Coronary Disease / Q000188:drug therapy* / Q000209:etiology* / Q000503:physiopathology; D005260:Female; D006801:Humans; D008297:Male; D009203:Myocardial Infarction / Q000188:drug therapy / Q000517:prevention & control*; D017682:Myocardial Stunning / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism; D018384:Oxidative Stress; D011379:Prognosis; D017382:Reactive Oxygen Species / Q000378:metabolism*; D018570:Risk Assessment
chemical_list: D000975:Antioxidants; D017382:Reactive Oxygen Species