Aim: To investigate the role of nitric oxide (NO), nitric oxide synthase (NOS) and endothelin-1 (ET-1) in the pathogenesis of hypoxic pulmonary hypertension and inhibiting effects of L-Arginine.
Methods: 30 rats were divided into 3 groups, normal control group (group NC); Hypoxic group (group HP): exposed to 10% O2 8 h/day, 3 weeks; Hypoxic + L-arginine (group LT): fed L-arginine 200 mg/kg before hypoxia. After exposed to hypoxia 21 days, hemodynamics were measured. Lung speciments were examined by light and electronic microscopes and morphometric analysis. NO, ET-1 levels in lung tissue were measured, the cNOS quantitative in the pulmonary endothelium were examined.
Results: In HP group, the mean pulmonary arterial pressure (m PAP), pulmonary vascular resistance (PVR) the percentage of completely muscular coattype medial muscle layer of pulmonary artery in intra-acine and ET-1 level of HP group increased (P < 0.01), but NO and cNOS level decreased (P < 0.01). Examined by electron micrograph, endothelium cells appeared swollen, broken and pealed of, basal lamina parted. The changes above in LT group reversed partly. But the changes above were still several than that of group NC (P < 0.05).
Conclusion: The structure remodel of pulmonary arteries and endothelium lesion in hypoxia cause m PAP, PVP arising, that are correlated with the levels of ET-1 increasing and NO, cNOS decreasing. For L-arginine can partly supply NO, it may partly reverse the changes of HPH.