| Abstract
| - Objective: Heat stress, with the expression of heat stress proteins, has been shown to protect the rabbit heart in vitro against global ischaemia/reperfusion injury, though no benefit is apparent in an in vivo rabbit model of infarct size. The aim of this study was therefore to investigate 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 stress could limit infarct size in the absence of blood, isolated buffer perfused 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 model in which a support rabbit (heat stressed or control) was used to perfuse the isolated heart. Results: In the buffer perfused heart, prior heat stress reduced I/R from 70.8(SEM 4.4)%, n=10, in controls to 51.5(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 stressed). If the perfusing rabbit had been heated, I/R was greater in both heat stressed and control hearts [51.9(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 effects, probably on the blood, which may override any benefit associated with myocardial stress protein synthesis. Cardiovascular Research 1993;27:962-967
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