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Antioxidant protection against damage during cardiac ischemia and reperfusion: effect of dimercapto-propanol.

Abstract
Oxygen-derived free radicals and their metabolites may contribute to the extension of cellular injury that occurs on reperfusion of the ischemic myocardium; and therapy directed against the toxic effects of reactive oxygen species has provided protection to the ischemic myocardium which undergoes subsequent reperfusion. We evaluated the effectiveness of dimercapto-propanol (1,2-dimercapto-propanol, British Anti-Lewisite, dimercaprol) to limit the extent of myocardial damage resulting from 60 minutes of severe ischemia followed by 30 minutes of reperfusion in the Langendorff-perfused rabbit heart. Dimercaptopropanol is a thiol agent, with two free sulfhydryl groups per molecule, which has no effect on glutathione status nor on the total tissue thiol pool. Pretreatment of the hearts with 10(-6) M dimercapto-propanol resulted in marked myocardial protection, measured in terms of preserved mechanical function and reduced creatine kinase release. On reperfusion less oxidative stress developed. The beneficial effects of dimercapto-propanol could not be explained by hemodynamic differences or effects on energy metabolism. In addition, it is unlikely that dimercapto-propanol acts as a free radical scavenger at the concentrations employed. The protection may be achieved by the drug keeping some key sulfhydryl groups of functional proteins in the reduced state.
AuthorsC Ceconi, S Curello, A Cargnoni, G M Boffa, R Ferrari
JournalCardioscience (Cardioscience) Vol. 1 Issue 3 Pg. 191-8 (Sep 1990) ISSN: 1015-5007 [Print] Italy
PMID2102808 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Free Radical Scavengers
  • Lactates
  • Sulfhydryl Compounds
  • Dimercaprol
  • Lactic Acid
  • Creatine Kinase
  • Glutathione
Topics
  • Animals
  • Creatine Kinase (metabolism)
  • Dimercaprol (therapeutic use)
  • Free Radical Scavengers
  • Glutathione (metabolism)
  • Lactates (metabolism)
  • Lactic Acid
  • Male
  • Mitochondria, Heart (physiology)
  • Myocardial Contraction (drug effects)
  • Myocardial Reperfusion
  • Myocardial Reperfusion Injury (prevention & control)
  • Myocardium (metabolism)
  • Premedication
  • Rabbits
  • Sulfhydryl Compounds (metabolism)
  • Time Factors

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