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1 Laboratoire HP2, Faculte de Medecine-Pharmacie, Grenoble, France
* To whom correspondence should be addressed. E-mail: christophe.ribuot{at}ujf-grenoble.fr.
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 KATP channel was also studied. Wistar male rats were exposed to IH (repetitive cycles of 1 min (40 s with FiO2 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 FiO2 10%. 24 h later their hearts were isolated and subjected to a 30-min no-flow global ischemia-120 min reperfusion sequence. For some hearts, L-NAME (a non-selective inhibitor of NOS) or 5-HD (a selective mitochondrial KATP blocker), was infused before ischemia. Infarct size (in % of ventricles) was significantly reduced by prior IH for 4 h (FiO2 10%) (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 to sham group. In contrast IH for 4 h (FiO2 5%) significantly increased infarct size (45.1 ± 3.6% vs 33.5 ± 2.5% in sham group). Acute IH for 4 h with a minimal FiO2 of 10% induced a delayed preconditioning against myocardial infarction in the rat, which was abolished by NOS inhibition and mitochondrial KATP channel blockade. Depth, duration and intermittence of hypoxia appeared to be critical for cardioprotection to occur.
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