The Role of Oxygen Free Radicals during the Course of Myocardial Ischemia/Reperfusion Injury: An Analysis and Critique

  • M. L. Hess
  • T. D. Greenfield
  • N. H. Manson
  • Eiichiro Okabe
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 86)


Myocardial ischemia results in a series of metabolic events that include the autooxidation of catecholamines, a reduction in intracellular pH, the breakdown of ATP to hypoxanthine and xanthine, an increase in reducing equivalents and activation of the cyclooxygenase system. All of these reactions favor the univalent reduction of molecular oxygen to free oxygen radicals and their metabolites (superoxide anion, ·O2 -, hydrogen peroxide, H2O2, and the hydroxyl radical, ·OH) (1,2). These metabolites of molecular oxygen are highly toxic and are capable of extensive tissue damage. With reperfusion and reintroduction of molecular oxygen into this previously ischemic vascular bed, the myocardium is then “primed” for the production of a “burst” of oxygen intermediates and further extensive tissue damage (3).


Xanthine Oxidase Oxygen Free Radical Phorbol Myristate Acetate Xanthine Dehydrogenase Arachidonic Acid Cascade 
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Copyright information

© Kluwer Academic Publishers 1988

Authors and Affiliations

  • M. L. Hess
    • 1
  • T. D. Greenfield
    • 2
  • N. H. Manson
    • 1
  • Eiichiro Okabe
    • 3
  1. 1.Department of Medicine, Division of CardiologyMedical College of VirginiaRichmondUSA
  2. 2.The Department of SurgeryMedical College of VirginiaRichmondUSA
  3. 3.The Department of PharmacologyKanagawa Dental CollegeYosukaJapan

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