Cardiac oxidase systems mediate oxygen metabolite reperfusion injury

J. M. Brown, M. A. Grosso, G. J. Whitman, L. S. Terada, J. E. Repine, A. H. Harken

Research output: Contribution to journalArticlepeer-review

3 Scopus citations


To investigate the mechanism of cardiac ischemia reperfusion injury, we fed rats tungsten (3 weeks) to inhibit molybdenum-dependent oxidase enzymes. Tungsten-treated isolated perfusion hearts (Langendorff, ventricular balloon, 37° C) had negligible xanthine oxidase activity (< 0.3 vs > 8.0 U/gm myocardium) and improved recovery of developed pressure (DP), contractility (+ dP/dt), and compliance (-dP/dt) after 20 minutes of global ischemia (37° C) and 40 minutes of reperfusion. Furthermore, the addition of dimethylthiourea, a freely diffusible O2 metabolite scavenger, but not equimolar urea, a non-O2 metabolite scavenger, improved recovery. High-dose urea improved recovery more than control but less than dimethylthiourea. Combining tungsten and equimolar urea improved recovery the same as dimethylthiourea. We conclude that: (1) inhibition of myocardial oxidase enzymes (including xanthine oxidase) improves recovery of ventricular function after ischemia and reperfusion in the isolated rat heart, (2) infusion (during reperfusion) of a permeable O2 metabolite scavenger (dimethylthiourea) but not equimolar urea improves recovery of ventricular function, (3) infusion of higher concentrations of urea improves postischemic function, and (4) myocardial reperfusion injury is distinguishable from ischemic injury.

Original languageEnglish (US)
Pages (from-to)266-271
Number of pages6
Issue number2
StatePublished - 1988
Externally publishedYes

ASJC Scopus subject areas

  • Surgery


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