HEAT-STRESS LIMITS INFARCT SIZE IN THE ISOLATED-PERFUSED RABBIT HEART

Objective: Heat stress, with the expression of heat stress proteins, h as been shown to protect the rabbit heart in vitro against global isch aemia/reperfusion injury, though no benefit is apparent in an in vivo rabbit model of infarct size. The aim of this study was therefore to i nvestigate this discrepancy and to discover whether heating itself has any effect which could negate the protection derived from myocardial stress protein synthesis. Methods: (1) To ascertain whether heat stres s could limit infarct size in the absence of blood, isolated buffer pe rfused hearts, with or without prior heat stress, were subjected to 45 min of regional ischaemia and 120 min reperfusion, and the resulting infarct size was expressed as a percentage of the risk area (I/R%). (2 ) The observations were repeated in an isolated blood perfused heart m odel in which a support rabbit (heat stressed or control) was used to perfuse the isolated heart. Results: In the buffer perfused heart, pri or heat stress reduced I/R from 70.8(SEM 4.4)%. n=10, in controls to 5 1.5(5.7)%, n=12 (p<0.05). In hearts perfused by support rabbits, prior heat stress reduced I/R [from 34.7(3.7)%, n=16, to 23.5(3.3)%, n=15 ( p<0.05)] only when the perfusing rabbit was a control (not heat stress ed). If the perfusing rabbit had been heated, I/R was greater in both heat stressed and control hearts [5 1.9(7.0)% and 44.9(3.3)%, p<0.05 v control support rabbit]. Conclusions: Heat stress limits infarct size in this rabbit model. However it appears to have additional adverse e ffects, probably on the blood, which may override any benefit associat ed with myocardial stress protein synthesis.