title: Heat stress-induced resistance to myocardial infarction in the isolated heart from transgenic [(mREN-2)27] hypertensive rats.
abstract: 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 HS-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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Laboratoire de Pharmacologie Cardiovasculaire Expérimentale-Biomolécules, Université Joseph Fourier, U.F.R. de Pharmacie, Grenoble, France.
authors.forename: M
authors.initials: M
authors.lastname: Joyeux
authors.forename: C
authors.initials: C
authors.lastname: Lagneux
authors.forename: G
authors.initials: G
authors.lastname: Bricca
authors.forename: D M
authors.initials: DM
authors.lastname: Yellon
authors.forename: P
authors.initials: P
authors.lastname: Demenge
authors.forename: C
authors.initials: C
authors.lastname: Ribuot
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D030801:Animals, Genetically Modified; D015153:Blotting, Western; D004591:Electrophoresis, Polyacrylamide Gel; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000096:biosynthesis; D006973:Hypertension / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D006979:Hyperthermia, Induced; D008297:Male; D009203:Myocardial Infarction / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins