title: Heat-shock response is associated with enhanced postischemic ventricular recovery.
abstract: In cells, hyperthermia induces synthesis of heat-shock proteins and the acquisition of thermotolerance. Thermotolerant cells are resistant to subsequent oxidative stress. In this study, heat-shocked hearts were examined for evidence of protection during ischemia and reperfusion. Rats were exposed to 15 minutes of 42 degrees C hyperthermia. Twenty-four hours later their hearts were isolated and perfused and the contractility examined during and after ischemic perfusion. No protection was observed during ischemic perfusion. However, upon reperfusion heat-shocked hearts had recovery of contractility within 5 minutes of reperfusion, while control hearts showed no contractility at this time. Throughout 30 minutes of reperfusion heat-shocked hearts had significantly improved recovery of contractile force, rate of contraction and rate of relaxation. Creatine kinase release, associated with reperfusion injury, was significantly reduced from a high of 386.8 +/- 78.9 mU/min/g heart wt for controls to 123.7 +/- 82.9 mU/min/g heart wt for heat-shocked hearts at 5 minutes of reperfusion. Following 30 minutes of reperfusion, ultrastructural examination revealed less damage of mitochondrial membranes in the heat-shocked hearts. Further biochemical investigations revealed that the antioxidative enzyme, catalase, was significantly increased to 137 +/- 12.7 U/mg protein in the heat-shocked hearts while the control value was 64.8 +/- 8.3 U/mg protein. Hyperthermic treatment, which induces the heat-shock response, may be therapeutic for salvaging ischemic myocardium during reperfusion, through a mechanism involving increased levels of myocardial catalase.
authors.affiliation: Department of Anatomy, Dalhousie University, Halifax, Nova Scotia, Canada.
authors.forename: R W
authors.initials: RW
authors.lastname: Currie
authors.forename: M
authors.initials: M
authors.lastname: Karmazyn
authors.forename: M
authors.initials: M
authors.lastname: Kloc
authors.forename: K
authors.initials: K
authors.lastname: Mailer
mesh_terms: D000818:Animals; D003327:Coronary Disease / Q000201:enzymology / Q000473:pathology / Q000503:physiopathology*; D003402:Creatine Kinase / Q000378:metabolism; D004591:Electrophoresis, Polyacrylamide Gel / Q000379:methods; D006321:Heart / Q000503:physiopathology*; D006352:Heart Ventricles; D006358:Hot Temperature; D066298:In Vitro Techniques; D008297:Male; D008854:Microscopy, Electron; D008929:Mitochondria, Heart / Q000648:ultrastructure; D009200:Myocardial Contraction; D009206:Myocardium / Q000201:enzymology / Q000648:ultrastructure; D010088:Oxidoreductases / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012769:Shock / Q000503:physiopathology*
chemical_list: D010088:Oxidoreductases; D003402:Creatine Kinase