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The Post Treatment Experiment: An Operational Definition of Reperfusion Injury

  • Charles F. Babbs
Part of the Basic Life Sciences book series (BLSC, volume 49)

Abstract

During the past few years evidence for a remarkable hypothesis about the pathophysiology of ischemia and reperfusion has begun to accumulate.1–5 The hypothesis states that significant tissue damage resulting from a period of tissue ischemia, followed by reperfusion, may actually occur during the reperfusion phase, rather than during the period of ischemia, and may be caused by oxyen-derived free radicals. This concept has been described as the oxygen paradox,6, 7 namely, that although restoration of oxygen supply to ischemic tissue is necessary for return of normal function, oxygen may simultaneously participate in certain deleterious chemical reactions. Such paradoxical oxygen toxicity occurring during reperfusion involves, not molecular oxygen, but rather the partially reduced oxygen species: superoxide anions, hydrogen peroxide, and hydroxyl radicals. These species are capable of initiating chain reactions that chemically modify cellular proteins, lipids, and amino acids to produce what is referred to as reperfusion injury.

Keywords

Reperfusion Injury Reperfusion Phase Total Circulatory Arrest Initiate Chain Reaction Significant Tissue Damage 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Plenum Press, New York 1988

Authors and Affiliations

  • Charles F. Babbs
    • 1
  1. 1.Biomedical Engineering CenterPurdue UniversityWest LafayetteUSA

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