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Existence and participation of xanthine oxidase in reperfusion injury of ischemic rabbit myocardium.

Abstract
Using a highly specific assay that minimizes enzyme inactivation in vitro, we found that rabbit myocardial tissue contained low levels of xanthine oxidase (XO) and xanthine dehydrogenase (XD) activity that were effectively inhibited by pretreatment of hearts with allopurinol. In parallel, allopurinol treatment also improved ventricular developed pressure, peak systolic pressure, and coronary flow in isolated hearts subjected to 30 min of normothermic global ischemia and 30 min of reperfusion. Although function was protected by allopurinol treatment, creatine kinase (CK) release was not altered by allopurinol. Inhibition of myocardial XO with allopurinol did not increase myocardial ATP or phosphocreatine. In addition, allopurinol did not scavenge superoxide anion or hydrogen peroxide in vitro. The results support the possibility that relatively low amounts of XO activity, similar to levels reported in human myocardium, may contribute to cardiac ischemia-reperfusion injury.
AuthorsL S Terada, J D Rubinstein, E J Lesnefsky, L D Horwitz, J A Leff, J E Repine
JournalThe American journal of physiology (Am J Physiol) Vol. 260 Issue 3 Pt 2 Pg. H805-10 (Mar 1991) ISSN: 0002-9513 [Print] UNITED STATES
PMID2000975 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
Chemical References
  • Free Radical Scavengers
  • Allopurinol
  • Hydrogen Peroxide
  • Xanthine Oxidase
  • Creatine Kinase
  • Oxygen
Topics
  • Allopurinol (metabolism, pharmacology)
  • Animals
  • Coronary Disease (enzymology, physiopathology)
  • Creatine Kinase (metabolism)
  • Free Radical Scavengers
  • Heart (physiopathology)
  • Hydrogen Peroxide (metabolism)
  • Myocardial Reperfusion Injury (enzymology)
  • Myocardium (enzymology)
  • Oxygen (metabolism)
  • Rabbits
  • Ventricular Function
  • Xanthine Oxidase (antagonists & inhibitors, metabolism)

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