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Acute intermittent hypoxia improves rat myocardium tolerance to ischemia

Laboratoire HP2, Hypoxie Physio-Pathologie Respiratoire et Cardiovasculaire, Equipe d’Accueil Ministère de la Recherche, Equipe Soutenue par la Région et l’Institut National de la Santé et de la Recherche Médicale, Faculté de Médecine-Pharmacie, Université Grenoble I, La Tronche, France

Submitted 18 January 2005 ; accepted in final form 3 May 2005

In this study, we investigated the influence of depth and duration of intermittent hypoxia (IH) on the infarct size development in isolated rat heart. The role of nitric oxide synthase (NOS) and ATP-sensitive K⁺ (K_ATP) channel was also studied. Wistar male rats were exposed to IH [repetitive cycles of 1 min, 40 s with inspired oxygen fraction (FI_O2), 5 or 10%, followed by 20-s normoxia], during 30 min or 4 h. Another group was exposed to 4 h of continuous hypoxia with 10% FI_O2. Twenty-four hours later, their hearts were isolated and subjected to a 30-min no-flow global ischemia-120-min reperfusion sequence. For some hearts, N-nitro-L-arginine methyl ester (L-NAME) (a nonselective inhibitor of NOS) or 5-hydroxydecanoic acid (5-HD) (a selective mitochondrial K_ATP blocker) was infused before ischemia. Infarct size (in percentage of ventricles) was significantly reduced by prior IH for 4 h (10% FI_O2) (21.8 ± 3.1 vs. 33.5 ± 2.5% in sham group). This effect was abolished by L-NAME or 5-HD. Infarct size was not different in groups subjected to either 30 min of IH or to continuous hypoxia compared with sham group. In contrast, IH for 4 h (5% FI_O2) significantly increased infarct size (45.1 ± 3.6 vs. 33.5 ± 2.5% in sham group). Acute IH for 4 h with a minimal FI_O2 of 10% induced a delayed preconditioning against myocardial infarction in the rat, which was abolished by NOS inhibition and mitochondrial K_ATP channel blockade. Depth, duration, and intermittence of hypoxia appeared to be critical for cardioprotection to occur.

ischemia-reperfusion; infarction; K_ATP channel; nitric oxide

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