Free-radical scavengers preserve wall motion in the xanthine oxidase-deficient rabbit heart

Abstract

We investigated the role of free radicals in postischemic segmental dysfunction in the rabbit, a species that, like the human, has undetectable amounts of xanthine oxidase in its heart. Open-chest anesthetized rabbits were instrumented with 0.5-mm diameter sonomicrometer crystals to measure myocardial segment shortening. Occlusion of a left coronary branch for 20 minutes caused dyskinesis in the field of the occluded artery, but after reperfusion, over 40% of that function returned. Although either 15,000 U/kg body weight of human recombinant superoxide dismutase (hSOD) alone or 5000 U/kg of catalase alone (each infused intravenously over 90 minutes starting 15 minutes before occlusion) failed to improve postischemic segmental shortening, the combination of hSOD and catalase did improve postischemic shortening. Most hearts had small infarcts. Analysis of the relationship between infarct size and regional function indicated that infarction alone could not account for all of the dysfunction and that some stunning must have been present. Whether the combination of hSOD and catalase improved wall motion by reducing infarct size or reducing stunning could not be determined. We conclude that rabbit heart is similar to dog heart in that free radicals contribute to postischemic dysfunction, but that rabbit heart is more resistant to stunning.