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1 Laboratoire HP2, Physio-Pathologie Respiratoire et Cardiovasculaire, Faculte de Medecine-Pharmacie, Universite Grenoble I, 38 706 La Tronche, France
* To whom correspondence should be addressed. E-mail: marie.faure{at}ujf-grenoble.fr.
Coronary heart disease (CHD) is frequently associated with obstructive sleep apnea (OSA) syndrome and treating OSA appears to significantly improve the outcome in CHD. Thus, we have developed a rat model of chronic intermittent hypoxia (IH) in order to study the influence of this condition on myocardial ischemia-reperfusion tolerance and on functional vascular reactivity. Wistar male rats were divided in 3 experimental groups (n = 12 each) subjected to chronic intermittent hypoxia (IH group), normoxia (N group) or control conditions (control group). IH consisted of repetitive cycles of 1 min (40 s with FiO2 5% followed by 20 s normoxia) and was applied for 8 h during daytime, for 35 days. Normoxic cycles were applied in the same conditions, FiO2 remaining constant at 21%. On day 36, mean arterial blood pressure (MABP) was measured before isolated hearts were submitted to an ischemia-reperfusion protocol. The thoracic aorta and left carotid artery were also excised for functional reactivity studies. MABP was not significantly different between the three experimental groups. Infarct sizes (in % of ventricles) were significantly higher in IH group (46.9 ± 3.6%) compared to N (26.1 ± 2.8%) and control (21.7 ± 2.1%) groups. Vascular smooth muscle function was similar in aorta and carotid arteries from all groups. The endothelium-dependent relaxation in response to acetylcholine was also similar in aorta and carotid arteries from all groups. Chronic IH increased heart's sensitivity to infarction, independently of a significant increase in MABP, and did not affect vascular reactivity of aorta and carotid arteries.
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