© 1999 by European Society of Cardiology
Copyright © 1999, European Society of Cardiology
Heat stress fails to protect myocardium of streptozotocin-induced diabetic rats against infarction
aLaboratoire de Pharmacologie Cardiovasculaire Expérimentale-Biomolécules, Université Joseph Fourier, U.F.R. de Pharmacie, Grenoble, France
bLaboratoire de Biologie du Stress Oxydant, Université Joseph Fourier, U.F.R. de Pharmacie, Grenoble, France
cThe Hatter Institute for Cardiovascular Studies, University College London Hospitals & Medical School, London, UK
* Corresponding author. Corresponding address: Laboratoire de Pharmacologie, Faculté de Pharmacie, Domaine de la Merci, 38706 La Tronche Cedex, France. Tel.: +33-476-637-108; fax: +33-476-637-152 Christophe.Ribuot{at}ujf-grenoble.fr
Objective: Protection conferred by heat stress (HS) against ischaemia–reperfusion injury, in term of mechanical function and myocardial necrosis, has been extensively studied. In contrast, the effects of disease states on this HS-induced cytoprotective response are less known. Therefore, we investigated the effects of prior heat stress on the infarct size in the isolated heart and on the myocardial heat stress protein (HSP) 72 synthesis, in a model of insulin-dependent diabetic rats. Methods: Three groups of animals were studied: D rats were rendered diabetic by 55 mg/kg streptozotocin i.v. injection, DI rats received the same treatment plus a daily injection of insulin 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°C for 15 min) or sham-anaesthetised. Twenty-four hours later, their hearts were isolated, perfused using the Langendorff technique, and subjected to a 30 min occlusion of the left coronary artery followed by 120 min of reperfusion. Myocardial HSP72 content was measured 24 h after HS or sham treatment using an electrophoresis coupled with a Western blot analysis. Results: Infarct-to-risk ratio (I/R) was significantly reduced in hearts from heat-stressed (11.7±2.0%) 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%) rats. Risk zones were similar between all experimental groups. The incidence of ventricular arrhythmias during ischaemia and reperfusion periods was not different between the six experimental groups. Western blot analysis of the myocardial HSP72 content showed a comparable heat stress-induced increase of this protein, in V, D and DI animals. Conclusion: These results demonstrate that myocardial protective effect induced by heat stress could not extend to a pathological animal model like the diabetic rat and seems to be unrelated to the HSP72 level. Further investigations are required to elucidate the precise role of the heat stress proteins in this adaptive response.
KEYWORDS Heat stress; Infarct size; Diabetic rats; Streptozotocin; Heat stress protein
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