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Pathophysiology of Anthracycline-Induced Cardiomyopathy

  • C. W. Tomlinson
  • J. H. McNeill
  • D. V. Godin
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 65)

Abstract

The pathophysiological events leading to anthracycline cardiomyopathy remain unclear in spite of intensive investigations. Major factors are thought to include stimulation of chemical processes giving rise to superoxide or hydroxyl radicals capable of causing oxidative damage to cellular membranes and thereby changes in subcellular organelles (1,2). It has also been suggested that anthracycline toxicity may arise from increased myocardial permeability resulting from induced deficiency of protective mechanisms. This could be reflected by an alterations in such enxymes as catalase, superoxide dismutase and glutathione peroxidase (3,4,5).

Keywords

Sarcoplasmic Reticulum Ouabain Binding Adriamycin Treatment Ouabain Binding Site Myocardial Tissue Sample 
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

© Martinus Nijhoff Publishing, Boston 1987

Authors and Affiliations

  • C. W. Tomlinson
    • 1
    • 2
    • 3
  • J. H. McNeill
    • 1
    • 2
    • 3
  • D. V. Godin
    • 1
    • 2
    • 3
  1. 1.Departments of Medicine (Division of Cardiology), and PharmacologyUniversity of British ColumbiaVancouverCanada
  2. 2.Therapeutics, Faculty of Medicine and Division of PharmacologyUniversity of British ColumbiaVancouverCanada
  3. 3.Toxicology, Faculty of Pharmaceutical SciencesUniversity of British ColumbiaVancouverCanada

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