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Cardiovascular Research 2003 58(1):118-125; doi:10.1016/S0008-6363(02)00812-X
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

iNOS is a mediator of the heat stress-induced preconditioning against myocardial infarction in vivo in the rat

Claire Arnauda, Diane Godin-Ribuota, Serge Bottaria, André Peinnequinb, Marie Joyeuxa, Pierre Demengea and Christophe Ribuota,*

aLaboratoire Stress Cardiovasculaires et Pathologies Associées, Faculté de Pharmacie, Domaine de la Merci, 38706 La Tronche, France
bLaboratoire Radiobiologie et Inflammation, Centre de Recherche du Service de Santé des Armées (CRSSA), Emile Parde, Grenoble, France

* Corresponding author. Tel.: +33-476-637-108; fax: +33-476-637-152. christophe.ribuot{at}ujf-grenoble.fr

Objective: The inducible isoform of nitric oxide synthase (iNOS) is known to be a trigger of the heat stress (HS)-induced cardioprotection. Since iNOS also appears to mediate various forms of myocardial preconditioning, the goal of this study was to investigate its role as a mediator of the HS response. Methods and Results: Male Wistar rats were divided in six groups, subjected or not to HS (42°C internal temperature, for 15 min). Twenty-four hours later, they were treated or not with either L-NAME, a non-selective inhibitor of NO synthase isoforms, or 1400W, a selective iNOS inhibitor, 10 min before being subjected to a 30-min left coronary artery occlusion followed by a 120-min reperfusion, in vivo. The infarct size (tetrazolium staining) reducing effect conferred by heat stress (from 46.0±1.4% in sham to 26.8±3.8% in HS groups) was completely abolished by both L-NAME (53.9±3.1%) and 1400W (51.8±3.3%). Additional studies using Western blot analysis demonstrated a 3.8-fold increase in myocardial iNOS protein expression 24 h after HS. Conclusion: These results suggest an involvement of iNOS as a mediator of the protection conferred by heat stress against myocardial ischaemia.

KEYWORDS eNOS, endothelial nitric oxide synthase; HS, heat stress; Hsp, heat stress protein; I, infarct zone; IL-1β, interleukin-1β; iNOS, inducible nitric oxide synthase; IP, ischaemic preconditioning; KATP channel, ATP-dependent potassium channel; LCA, left coronary artery; L-NAME, nitro-L-arginine-methylester; LV, left ventricle; MAP, mean arterial blood pressure; NO, nitrite oxide; p38 MAP, p38 mitogen activated protein; PKC, protein kinase C; R, risk zone; ROS, reactive oxygen species; TNF-{alpha}, tumor necrosis factor-{alpha}; 1400W, N-[(3-aminoethyl)benzyl] acetamidine


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