Myocardial Protection with Blood Cardioplegia in Ischemically Injured Hearts: Reduction of Reoxygenation Injury with Allopurinol

Abstract

Myocellular injury mediated by oxygen radicals potentially limits myocardial protection in ischemically damaged hearts. This damage may be greater with oxygen-carrying blood cardioplegic solutions. A major mechanism of oxygen radical production is the conversion of hypoxanthine to uric acid by xanthine oxidase. In 16 anesthetized dogs, we studied whether adding allopurinol, a xanthine oxidase inhibitor, to blood cardioplegia would improve recovery of left ventricular (LV) performance and oxygen consumption. Millar transducer-tipped catheters and minor axis ultrasonic crystals were placed to assess LV performance by the slope of the end-systolic pressure-minor axis diameter relationships (E max). Following total vented bypass, the hearts underwent 30 minutes of normothermic ischemia and then hypothermic blood cardioplegia with 1 mM allopurinol (N = 8) or without allopurinol (N = 8). Postischemic LV performance was significantly better with allopurinol than without (49.5 ± 8.0 versus 17.4 ± 4.1% of preischemic E max; p < 0.004). Postischemic LV oxygen consumption in the beating working state, calculated from LV blood flow (15-μm microspheres) and oxygen extraction, was comparable to preischemic values with and without allopurinol (10.2 ± 1.2 versus 8.6 ± 1.2 ml O 2/100 gm/min). We conclude that allopurinol enhancement of blood cardioplegia increases myocardial protection in severely ischemic ventricles.