Heat stress fails to protect myocardium of streptozotocin-induced diabeticrats against infarction

Objective: Protection conferred by heat stress (HS) against ischaemia-reper fusion injury, in term of mechanical function and myocardial necrosis, has been extensively studied. In contrast, the effects of disease states on thi s MS-induced cytoprotective response are less known. Therefore, we investig ated the effects of prior heat stress on the infarct size in the isolated h eart and on the myocardial heat stress protein (HSP) 72 synthesis, in a mod el of insulin-dependent diabetic rats. Methods: Three groups of animals wer e studied: D rats were rendered diabetic by 55 mg/kg streptozotocin i.v. in jection, DI rats received the same treatment plus a daily injection of insu lin started 2 weeks after and V rats received the vehicle of streptozotocin plus a daily injection of saline. Eight weeks later, D, DI and V rats were either heat-stressed (42 degrees C for 15 min) or sham-anaesthetised. Twen ty-four hours later, their hearts were isolated, perfused using the Langend orff technique, and subjected to a 30 min occlusion of the left coronary ar tery followed by 120 min of reperfusion. Myocardial HSP72 content was measu red 24 h after HS or sham treatment using an electrophoresis coupled with a Western blot analysis. Results: Infarct-to-risk ratio (I/R) was significan tly reduced in hearts from heat-stressed (11.7+/-2.08) compared to sham (30 .0+/-3.2%)V rats. This cardioprotection was not observed in hearts from D ( I/R: 31.4+/-3.3 vs. 34.3+/-3.5%) and DI (I/R: 28.7+/-1.6 vs. 30.3+/-1.6%) r ats. Risk zones were similar between all experimental groups. The incidence of ventricular arrhythmias during ischaemia and reperfusion periods was no t different between the six experimental groups. Western blot analysis of t he myocardial HSP72 content showed a comparable heat stress-induced increas e of this protein, in V, D and DI animals. Conclusion: These results demons trate that myocardial protective effect induced by heat stress could not ex tend to a pathological animal model like the diabetic rat and seems to be u nrelated to the HSP72 level. Further investigations are required to elucida te the precise role of the heat stress proteins in this adaptive response. (C) 1999 Elsevier Science B.V. All rights reserved.