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Membrane Phospholipid Metabolism during Myocardial Ischemia: Mechanisms of Accumulation of Unesterified Arachidonate

  • K. R. Chien
  • L. M. Buja
  • J. T. Willerson

Abstract

Recent studies have suggested that alterations in membrane structure and function are causally related to the development of irreversible injury during myocardial ischemia (1–4). In an ischemic canine myocardial model, studies by Jennings et al. have demonstrated the presence of sarcolemmal membrane defects by electron microscopy which correlate with the time course of the onset of irreversible injury and the accumulation of tissue calcium (1). Studies in a perfused rabbit septal model (4) have correlated the decrease in myocardial contractile performance during ischemia with the development of increased sarcolemma1 membrane cation permeability (4). Calcium blocking agents have been demonstrated to have protective effects on the development of irreversible injury in calcium accumulation during myocardial ischemia (5, 6). Acute myocardial infarction in man is characterised by leakage of cytosolic enzymes across the sarcolemmal membrane and into the intravascular space (7). In addition, the accumulation of technetium-99m pyrophosphate, a marker of a sarcolemmal membrane calcium permeability defect (8), is a sensitive marker of myocardial cell injury in clinical and animal studies (9).

Keywords

Membrane Phospholipid Irreversible Injury Sarcolemmal Membrane Beta Oxidation Dial Ischemia 
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 1984

Authors and Affiliations

  • K. R. Chien
    • 1
  • L. M. Buja
    • 1
  • J. T. Willerson
    • 1
  1. 1.Department of Internal Medicine (Cardiovascular Division)The University of Texas Health Science CenterDallasUSA

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