Reperfusion injury

John T. Flaherty, Myron L. Weisfeldt

Research output: Contribution to journalArticle


Several lines of evidence point to a major role of oxygen free radicals in the pathogenesis of cell death or dysfunction in a variety of disease processes. Recent studies from this as well as other laboratories have demonstrated that oxygen free radicals play a major role in the pathogenesis of post-ischemic reperfusion injury in the heart.1-4 We have recently developed methods for direct measurement of radical species and/or specific byproducts of radical injury.5 Timely administration of oxygen radical scavengers reduced the quantity of free radicals generated following reperfusion and in addition improved recovery of post-ischemic ventricular function and metabolism.3,6 In a regionally ischemic model the free radical scavenger recombinant human superoxide dismutase also administered at the time of reflow was shown to limit infarct size.4 In this article we review the biophysical and molecular mechanisms of oxygen free radical generation that are viewed as contributing to post-ischemic reperfusion injury. We also discuss the mechanisms by which the body defends against free radical attack and the interrelationship of free radical injury to other mechanisms of tissue injury.

Original languageEnglish (US)
Pages (from-to)409-419
Number of pages11
JournalFree Radical Biology and Medicine
Issue number5-6
StatePublished - 1988



  • Free radical scavengers
  • Hydroxyl radicals
  • Myocardial reperfusion injury
  • Oxygen free radicals
  • Superoxide dismutase
  • Superoxide radicals

ASJC Scopus subject areas

  • Biochemistry
  • Physiology (medical)

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