HEAT-STRESS ATTENUATES FREE-RADICAL RELEASE IN THE ISOLATED-PERFUSED RAT-HEART

Prior heat stress leads to an enhancement of postischemic mechanical f unction and improvement in biochemical indices of injury in the rat he art, associated with an elevation in endogenous catalase activity. We have examined the effect of heat stress on free radical release during reperfusion in the isolated rat heart using electron spin resonance ( ESR). Twenty four hours after heat stress or sham treatment, hearts we re perfused in the Langendorff mode and subjected to 10 min of no-flow global ischemia followed by 10 min of reperfusion. Coronary effluent was collected at specific time points in PBN for ESR measurement. A PB N adduct was identified with characteristics consistent with an alkoxy l radical: PBN-LO.. In sham hearts there was a rapid rise in adduct re lease to a maximum (228 +/- 15% of stabilization values, p < .05) occu rring 1 min into reperfusion. In heat stress hearts there was no signi ficant rise in adduct release during the reperfusion period. Pretreatm ent of hearts with 3-amino triazole, an inhibitor of catalase, failed to clarify whether the protection seen in heat stress hearts was a res ult of the elevation in catalase activity. These results suggest that heat stress protects the myocardium against the oxidative stress of is chemia-reperfusion.