Heat stress-induced resistance to myocardial infarction in the isolated heart from transgenic [(mREN-2)27] hypertensive rats.
124 - 130.
Objective: Heat stress (HS) is known to confer protection against ischaemia-reperfusion injury, including mechanical dysfunction and myocardial necrosis. However, the effects of disease states on this MS-induced cytoprotective response are less known. Therefore, we investigated the effects of prior heat stress on the infarct size in the isolated rat heart and on the myocardial heat stress protein (HSP) 72 synthesis, in transgenic [(mREN-2)27] hypertensive (TGH) rats or normotensive (NT) controls. Methods: TGH or NT rats were either heat stressed (42 degrees C for 15 min) or sham anaesthetised. After 24 h, their hearts were isolated, perfused using the Langengorff technique, and subjected to a 35-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 electrophoresis coupled with Western blot analysis. Results: Infarct-to-risk (I/R) ratio was significantly reduced in HS (15.5+/-1.2%) compared to sham (42.2+/-2.1%) hearts of NT rats. This reduction in infarct size was maintained in TGH hearts (I/R: 20.0+/-1.0 vs. 48.0+/-3.8%). Risk zones were similar between all experimental groups. The incidence of ventricular arrhythmias during ischaemia and reperfusion periods was not different between the four experimental groups. Western blot analysis of the myocardial HSP72 content showed a heat stress-induced increase of this protein, in both TGH and NT animals. Conclusion: These results demonstrate that the myocardial protective effect induced by heat stress could extend to a pathological animal model like the transgenic [(mREN-2)27] hypertensive rat and is correlated with a myocardial HSP72 induction. (C) 1998 Elsevier Science B.V. All rights reserved.
|Title:||Heat stress-induced resistance to myocardial infarction in the isolated heart from transgenic [(mREN-2)27] hypertensive rats|
|Keywords:||heat stress, infarct size, transgenic [(mREN-2)27] hypertensive rats, heat stress protein, ISCHEMIC PRECONDITIONING PROTECTS, DELAYED PROTECTION, SHOCK PROTEIN-72, GENE, REPERFUSION, HYPERTROPHY, INDUCTION, BLOCKADE, RABBIT, INJURY|
|UCL classification:||UCL > School of Life and Medical Sciences
UCL > School of Life and Medical Sciences > Faculty of Population Health Sciences
UCL > School of Life and Medical Sciences > Faculty of Population Health Sciences > Institute of Cardiovascular Science
UCL > School of Life and Medical Sciences > Faculty of Population Health Sciences > Institute of Cardiovascular Science > Hatter Cardiovascular Institute
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