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目的 :探讨结构型一氧化氮合酶 (cNOS)、一氧化氮 (NO)、内皮素 1(ET 1)在低氧性肺动脉高压 (HPH)发病中的机制及左旋精氢酸 (L Arg)对HPH的治疗作用。 方法 :30只健康雄性SD大鼠平均分为三组 :正常对照组 (NC组 )、低氧组 (HP组 )、低氧左旋精氨酸治疗组 (LT组 )。后组每日低氧前给予 2 0 0mg/kgL Arg。于低氧 2 1d检测动物血流动力学 ,肺组织NO、ET 1含量 ,肺动脉内皮cNOS含量的改变 ,光镜及电镜观察肺小动脉形态学改变。结果 :HP组平均肺动脉压 (mPAP)、肺血管阻力 (PVR)、腺泡内环肌型肺小动脉百分比、中膜厚度百分比及肺组织ET 1含量较NC组增高 (P <0 .0 1)、肺动脉内皮cNOS、肺组织NO含量较NC组明显降低 (P <0 .0 1)。肺动脉内皮细胞损伤明显 ,LT组比HP组上述指标部分逆转 ,但与NC组相比仍有差异 (P <0 .0 5 )。结论 :慢性低氧可引起大鼠肺动脉结构重建及内皮损伤 ,致mPAP、PVR上升 ,且与肺组织ET 1升高、NO降低、肺动脉内皮cNOS含量下降相关 ,L Arg可部分逆转HPH病理生理改变 ,对HPH有一定治疗作用
Objective: To investigate the mechanism of structural nitric oxide synthase (cNOS), nitric oxide (NO) and endothelin 1 (ET 1) in the pathogenesis of hypoxic pulmonary hypertension (HPH) Therapeutic effect on HPH. Methods: Thirty healthy male Sprague - Dawley rats were equally divided into three groups: normal control group (NC group), hypoxic group (HP group) and hypoxic L - arginine treatment group (LT group). The latter group was given 200 mg / kg L Arg daily before hypoxia. The hemodynamics, contents of NO, ET 1 and cNOS in pulmonary artery were detected in hypoxia for 21 days. The morphological changes of pulmonary arterioles were observed by light microscope and electron microscope. Results: The mean pulmonary arterial pressure (mPAP), pulmonary vascular resistance (PVR), the percentage of pulmonary arteriolar pulmonary arterioles, the percentage of medial thickness and the content of ET 1 in lung tissue in HP group were higher than those in NC group (P <0.01) ), Pulmonary artery endothelium cNOS, lung tissue NO content was significantly lower than the NC group (P <0.01). The damage of pulmonary artery endothelial cells was obvious. The above indexes were partially reversed in LT group compared with HP group, but there was still significant difference compared with NC group (P <0.05). CONCLUSION: Chronic hypoxia can induce structural remodeling of pulmonary arteries and endothelial injury in rats, resulting in increased mPAP and PVR, which is associated with increased ET 1, decreased NO and decreased pulmonary cNOS content in lung tissue. L Arg partially reversed the pathophysiological changes of HPH HPH has a certain therapeutic effect