摘要
目的 :进一步了解西拉普利 (cilazapril)对缺氧大鼠肺血管内皮 (EC)功能失调的改善作用。方法 :采用生化、放射免疫、透射电镜和血流动力学技术研究缺氧肺血管EC结构和功能状况。结果 :(1)缺氧大鼠肺血管EC超微结构发生变化 ,细胞受损。 (2 )血管EC内皮依赖性舒缩功能失调 ,表现为血浆NO、SOD和肺组织eNOS显著降低 ,血浆ET - 1、ACE和MDA显著增加 ,这些舒缩因子与肺动脉平均压 (mPAP)呈显著正相关或负相关。 (3)cilazapril显著降低ET - 1水平和ACE活性 ,同时增加NO水平和eNOS及SOD活性 ,减轻EC结构受损。结论 :缺氧大鼠存在肺血管EC结构受损和功能失调是参与缺氧性肺动脉高压 (PH)发病机理之一。Cilazapril能够减轻EC的损伤 ,改善EC的分泌功能 。
AIM: To study the effect of cilazapril on pulmonary vascular endothelial dysfunction in hypoxic rats. METHODS: The structure and function of endothelium in hypoxic rats were studied by biochemical analysis, radioimmunoassay, transmission electron microscope and correlated with hemodynamic. RESULTS: 1) The change and damage of ultrastructure in endothelial cell (EC) were obsevered in hypoxic rats. 2) The contents of plasma nitric oxide (NO) and superoxide dismutase (SOD) activity in blood as well as endothelial nitric oxide synthase (eNOS) activity in the lung tissue were significantly lower in the hypoxic rat than those in contral animals. The concentrations of plasma endothelin-1(ET-1) and angiotensin converting enzyme(ACE) as well as malondialdehyde(MDA) were significantly higher in the hypoxic rat than these in contral animals. The relaxing and contracting factors had a significant positive/negative correlation with mean pulmonary artery pressure (mPAP). 3) Cilazapril significantly decreased the level of ET-1 and ACE and significantly increased the level of NO and activity of eNOS and SOD. At the same time, cilazapril extenuated hypoxia-induced injuries of EC. CONCLUSION: The results indicate that damaging structure and dysfunction of EC existes in hypoxic rats. The cilazapril effectively preventes and treates the chronic hypoxic PH by relieving the injury and improving secretion in EC.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2003年第12期1674-1679,共6页
Chinese Journal of Pathophysiology
关键词
缺氧
内皮
西拉普利
肺
Anoxia
Endothelium
Cilazapril
Lung
