Document Detail


Myocardial ischemia, reperfusion and free radical injury.
MedLine Citation:
PMID:  1692444     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Reperfusion of coronary arteries to limit myocardial ischemic injury and extent of myocardial necrosis is possible by either the use of fibrinolytic therapy, coronary angioplasty or coronary artery bypass surgery. The concept that early reperfusion may salvage jeopardized myocardium is derived from basic experimental studies which purported to demonstrate that the ultimate extent of irreversible myocardial injury could be reduced by reperfusion of the ischemic myocardium within 3 hours from the onset of regional myocardial ischemia. It is firmly established that salvage of ischemic myocardium is dependent on early restoration of blood flow to the myocardium at risk. Despite dependency on reoxygenation for ultimate survival, myocardial tissue that is reperfused and reoxygenated may be subjected to additional injurious insult due to reactive metabolites of oxygen. The cytotoxic species of oxygen are referred to as "oxygen free radicals." Coincident with the influx of inflammatory cells into the reperfused region is an additional loss of otherwise viable myocardial cells. There is strong support for the concept that the polymorphonuclear leukocyte is a contributor to the phenomenon of "reperfusion" or "reoxygenation" injury in the blood perfused heart. This discussion focuses on the role of the neutrophil as a potential contributor to the extension of tissue injury and reviews those interventions, which although in the experimental stage, offer promise of becoming therapeutically important in the future and may help elucidate the mechanisms underlying the potentially deleterious role of the neutrophil in situations involving whole blood reperfusion of the ischemic myocardium.
Authors:
B R Lucchesi
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.; Review    
Journal Detail:
Title:  The American journal of cardiology     Volume:  65     ISSN:  0002-9149     ISO Abbreviation:  Am. J. Cardiol.     Publication Date:  1990 May 
Date Detail:
Created Date:  1990-06-14     Completed Date:  1990-06-14     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0207277     Medline TA:  Am J Cardiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  14I-23I     Citation Subset:  AIM; IM    
Affiliation:
University of Michigan Medical School, Department of Pharmacology, Ann Arbor 48109-0626.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Adhesion Molecules / metabolism
Chemotactic Factors
Complement Activation
E-Selectin
Free Radicals
Humans
Ibuprofen / pharmacology
Intercellular Adhesion Molecule-1
Membrane Glycoproteins / metabolism
Myocardial Infarction / physiopathology*
Myocardial Reperfusion Injury / physiopathology*
Neutrophils / drug effects,  physiology*
Superoxide Dismutase / therapeutic use
Grant Support
ID/Acronym/Agency:
HL-19782-11/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Cell Adhesion Molecules; 0/Chemotactic Factors; 0/E-Selectin; 0/Free Radicals; 0/Membrane Glycoproteins; 126547-89-5/Intercellular Adhesion Molecule-1; 15687-27-1/Ibuprofen; EC 1.15.1.1/Superoxide Dismutase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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