Allopurinol enhanced adenine nucleotide repletion after myocardial ischemia in the isolated rat heart.

R D Lasley; S W Ely; R M Berne; R M Mentzer

doi:10.1172/JCI113288

Department of Physiology, University of Virginia School of Medicine, Charlottesville 22908.

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Department of Physiology, University of Virginia School of Medicine, Charlottesville 22908.

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Department of Physiology, University of Virginia School of Medicine, Charlottesville 22908.

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Department of Physiology, University of Virginia School of Medicine, Charlottesville 22908.

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Published in Volume 81, Issue 1 on January 1, 1988
J Clin Invest. 1988;81(1):16–20. https://doi.org/10.1172/JCI113288.
© 1988 The American Society for Clinical Investigation

Published January 1, 1988 - Version history

Allopurinol, a competitive inhibitor of xanthine oxidase, has been shown to have a protective effect on ischemic myocardium, but its mechanism of action remains controversial. We used an isolated rat heart preparation to test the hypothesis that allopurinol could restore adenosine triphosphate (ATP) levels and improve the recovery of left ventricular function after global myocardial ischemia. Hearts were equilibrated for 30 min, subjected to 10 min of global, normothermic (37 degrees C) ischemia, and reperfused for 15, 30, and 60 min. Hearts treated with allopurinol (100 microM) exhibited greater ATP levels and improved function during reperfusion than did untreated control hearts. Hearts treated with hypoxanthine (100 microM), the substrate for xanthine oxidase, also showed increased ATP and functional recovery compared with controls. These results suggest that allopurinol may protect the globally ischemic myocardium by enhancing the salvage of hypoxanthine for reincorporation into adenine nucleotides.

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