title: Free-radical production triggered by hyperthermia contributes to heat stress-induced cardioprotection in isolated rat hearts.
abstract: 1. Heat stress (HS) is known to protect the myocardium against ischaemic damage. It has been reported that reactive oxygen species (ROS) are abundantly produced during this stress. Since mechanisms triggering the HS-induced cardioprotection remain unknown, we investigated the role of ROS in the genesis of this protective phenomenon. 2. Rats were divided into four groups (n=8 in each group), subjected to either hyperthermia (42 degrees C internal temperature for 15 min) or sham anaesthesia and treated or not with N-2-mercaptopropionyl glycine (MPG), a synthetic antioxidant, 10 min before HS. Twenty-four hours later, their hearts were isolated, retrogradely perfused, and subjected to a 30-min occlusion of the left coronary artery followed by 120 min of reperfusion. Myocardial Hsp 27 and 70 expression was assessed by Western blot analysis (n=4). Cardiac activities of antioxidant enzymes (superoxide dismutase and glutathione peroxidase) were also examined (n=4). 3. Infarct-to-risk zone ratio was significantly reduced in HS (17+/-1.3%) compared to Sham (34.3+/-1.7%) hearts. This effect was abolished by MPG pretreatment (40.6+/-1.9% in HS+MPG vs. 39.8+/-2.5% in Sham+MPG hearts). This cardioprotection was associated with an enhanced Hsp 27 and 70 expression, which was not modified by MPG pretreatment. Antioxidant enzyme activities was not modified by heat stress or MPG pretreatment. 4. Free radical production following hyperthermia appears to play a role in the heat stress induced cardioprotection, independently of Hsp levels. Antioxidant enzyme activities do not seem to be implicated in this cardioprotective mechanism.
authors.affiliation: Laboratoire Stress Cardiovasculaires et Pathologies Associées, Faculté de Pharmacie, Domaine de la Merci, 38706 La Tronche, France.
authors.forename: Claire
authors.initials: C
authors.lastname: Arnaud
authors.forename: Marie
authors.initials: M
authors.lastname: Joyeux
authors.forename: Catherine
authors.initials: C
authors.lastname: Garrel
authors.forename: Diane
authors.initials: D
authors.lastname: Godin-Ribuot
authors.forename: Pierre
authors.initials: P
authors.lastname: Demenge
authors.forename: Christophe
authors.initials: C
authors.lastname: Ribuot
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D015153:Blotting, Western; D005334:Fever / Q000378:metabolism; D005609:Free Radicals / Q000378:metabolism*; D005979:Glutathione Peroxidase / Q000378:metabolism; D055551:HSP27 Heat-Shock Proteins; D018840:HSP70 Heat-Shock Proteins / Q000032:analysis; D018882:Heat Stress Disorders / Q000150:complications / Q000378:metabolism*; D006360:Heat-Shock Proteins; D006439:Hemodynamics / Q000187:drug effects; D066298:In Vitro Techniques; D008297:Male; D009203:Myocardial Infarction / Q000209:etiology; D009206:Myocardium / Q000378:metabolism*; D009363:Neoplasm Proteins / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D005609:Free Radicals; D055551:HSP27 Heat-Shock Proteins; D018840:HSP70 Heat-Shock Proteins; D006360:Heat-Shock Proteins; C486114:Hspb1 protein, rat; D009363:Neoplasm Proteins; D017382:Reactive Oxygen Species; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase