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Background: Intermittent hypoxia has been shown to provide myocardial protection against ischemia/reperfusion injury. Cardiac myocyte loss through apoptosis has been reported in ischemia/reperfusion injury. The role of nitric oxide (NO) in modulating apoptosis in rats exposed to chronic intermittent hypoxia is controversial. The aim of the present work is to investigate the possible role of nitric oxide synthase inhibition on modulation of apoptosis in ischemicreperfused isolated hearts of rats exposed to chronic intermittent hypoxia. Methods: Adult male albino rats were used and exposed to normaxic or hypoxic conditions as follows: Group I: Normoxic conditions (normoxia group), Group II : Chronic intermittent hypoxia (CIH group) (10% O2 and 90% N2) for 8 hours daily, then to normal environmental air for the rest of the day, 5 days/ week for 4 weeks, Group III: Normoxic conditions and treated with L-NAME (10 mg/kg B.W. via intra-gastric route) (L-NAME group), Group IV: Chronic intermittent hypoxia and treated with L-NAME (CIH + L-NAME group) They had daily L-NAME(10 mg/kg B.W. via intra-gastric route) and exposed to the chronic intermittent hypoxia in the same way and duration as rats of group II. Isolated perfused hearts were subjected to 30 minutes of global ischemia followed by 30 minutes reperfusion. Left ventricular developed pressure (LVDP), contractility (dp/dt), and heart rate (HR) were recorded continuously. Expression of Bcl-2 in the myocardium was detected. Results: The parameters of functional recovery were improved in CIH group with significant increase in Bcl-2 expression as compared to normoxia group. Treatment with L-NAME led to attenuation of improved post– ischemic recovery of the ventricular function provided by chronic intermittent hypoxia with significant reduction in Bcl-2 expression compared with CIH group. Conclusion: adaptation to chronic intermittent hypoxia increases cardiac tolerance to ischemia/reperfusion. This protective effect was associated with increased expression of the antiapoptotic protein Bcl-2, that limits the apoptotic cell death in the myocardium following the ischemic/reperfusion insult. L-NAME attenuated both the improved recovery of cardiac function and the expression of antiapoptotic protein Bcl-2 induced by CIH.

bulletin of egyptian society for physiological sciences

Chronic Intermittent Hypoxia Protects the Rat Heart Against Ischemic/Reperfusion Injury by Modulating Apoptosis: A Possible Role for Endogenous Nitric Oxide