Study on sudden cardiovascular death in animal model of sleep apnea syndrome

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We have exploited apparatus that can expose many rats to intermittent hypoxia (IH) for a long period. IH for 3 weeks induces autophagy in the myocardium of the young rats, thereby preventing heart failure through degradation of injured organnels and degenerated proteins.In adult (9 month) but not young (2 month) rats, IH for 3 weeks induces pulmonary artery (PA) hypertension (PAH) through activation of arginase and reciprocal inhibition of nitric oxide (NO) synthase (NOS). In young rats, IH for 6 weeks induces recruitement of macrophage with enhanced expression of beta3-adrenergic receptor-inducible NOS around PAs. With sympathetic overdrive, the macrophage-derived NO prevents PAH. In young rats fed high fat diet, IH for 4-5days induced PAH through activation of endothelin or coagulation systems. Collectively, IH induces adaptative mechanisms to prevent heart failure or PAH in young and healthy arts, but IH exerts deleterious effects in adult and hyperlipidemic rats.