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Chronic Intermittent Hypobaric Hypoxia Ameliorates Pulmonary Hypertension Induced by Monocrotaline in Rats

The anti‐hypertensive effect of chronic intermittent hypobaric hypoxia (CIHH) has been demonstrated, but the effect of CIHH on pulmonary hypertension (PAH) is not elucidated. This study investigated the effect of CIHH on monocrotaline (MCT)‐induced PAH in rats. Adult male rats were randomly divided into control group, PAH group, CIHH group, and CIHH+MCT group. The CIHH rats were treated with a hypobaric hypoxia simulating 5000 m altitude for 28 days, 6 hours per day in a hypobaric chamber. The PAH rats were subjected to a single‐dose injection of MCT (60 mg/kg, intraperitoneally). The CIHH+MCT rats were subjected to 28‐days CIHH treatment before MCT injection. The pulmonary arterial pressure and right ventricular pressure were measure through catheterization, and the wall thickness of pulmonary artery and right ventricle were measured. Micro‐vascular tension recording technique was used to determine the relaxation in pulmonary arterioles. Western blot and quantitative PCR were used to determine the expression of eNOS protein and mRNA in pulmonary arterioles. The mean pulmonary artery pressure and right ventricular systolic pressure were increased in MCT‐treated rats but did not changed significantly in CIHH+MCT rats compared with control rats. The wall thickness of pulmonary arterial and right ventricle were significantly increased in MCT‐treated rats and these increases were smaller in rats treated with CIHH and MCT. The endothelial‐dependent and endothelial‐independent relaxation in pulmonary arterioles rings were significantly decreased in MCT‐treated rats compared with untreated rats. The decreased relaxation was significantly ameliorated by CIHH treatment. The expression levels of eNOS mRNA and protein in pulmonary arterioles were decreased in MCT‐treated rats compared with untreated rats and this downregulation of eNOS was prevented by CIHH treatment. In conclusion, CIHH ameliorates pulmonary hypertension in MCT‐treated rats. This effect may be is related to up‐regulation of eNOS by CIHH treatment.