Reperfusion injury after myocardial infarction: the role of free radicals and the inflammatory response.
Development of thrombolytic therapy as a treatment for myocardial infarction has focused attention on the events that occur upon reperfusion of ischemic myocardial tissue. Although it is well documented that salvage of the ischemic myocardium is dependent upon timely reperfusion, it is likely that the very events critical for survival may, in fact, lead to further tissue injury. A widely recognized source of reperfusion injury is the generation of oxygen-derived free radicals. These reactive oxygen species, which are formed within the first moments of reperfusion, are known to be cytotoxic to surrounding cells. In addition, strong support exists for the involvement of the inflammatory system in mediating tissue damage upon reperfusion. Coincident with the recruitment of neutrophils and activation of the complement system is an increase in the loss of viable cells. Although a number of mechanisms are likely to be involved in reperfusion injury, this discussion focuses on the roles that oxygen-derived free radicals and the inflammatory system play in mediating reperfusion injury.
Kilgore
K S
KS
Department of Pharmacology, University of Michigan Medical School, Ann Arbor 48109-0626.
Lucchesi
B R
BR
D002448:Cell Adhesion; D016923:Cell Death; D003165:Complement System Proteins / Q000276:immunology; D005609:Free Radicals / Q000378:metabolism*; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D009203:Myocardial Infarction / Q000150:complications*; D009504:Neutrophils / Q000502:physiology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D015427:Reperfusion Injury / Q000209:etiology* / Q000517:prevention & control; D013482:Superoxide Dismutase / Q000378:metabolism
D005609:Free Radicals; D017382:Reactive Oxygen Species; D003165:Complement System Proteins; D013482:Superoxide Dismutase