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肺动脉高压是高原心脏病的主要成因,同时也是决定其预后的关键因素。低压性缺氧所致的肺血管收缩及重构是慢性高原性肺动脉高压的主要原因。内皮是调节血管壁功能至关重要的结构,其功能的行使有许多需要通过一氧化氮(nitric ox-ide,NO)释放而介导,而NO与肺动脉高压的形成密切相关。肺血管NO主要由内皮一氧化氮合酶(endothelial nitric oxide synthase,e NOS)催化左旋精氨酸生成。他汀类药物近年被发现具有除调脂效应外的抗细胞增殖、免疫调节等作用,对e NOS-NO系统的调节亦为其作用途径之一。本文拟通过观察辛伐他汀对大鼠在模拟5 000m海拔高度的低压缺氧环境诱导的高原性肺动脉高压动
Pulmonary hypertension is the main cause of plateau heart disease, but also determines the prognosis of key factors. Pulmonary vasoconstriction and remodeling due to hypobaric hypoxia are the main causes of chronic high altitude pulmonary hypertension. Endothelium plays an important role in the regulation of vascular wall function. Many of its functions need to be mediated by the release of nitric oxide (NO), which is closely related to the formation of pulmonary hypertension. Pulmonary vascular NO mainly catalyzes the formation of L-arginine by endothelial nitric oxide synthase (eNOS). In recent years, statins have been found to have anti-cell proliferation and immunomodulatory effects besides the lipid-regulating effect, and the regulation of eNOS-NO system is also one of the ways of their actions. This paper intends to observe the simvastatin on rats in simulated low altitude hypoxia 5 000m hypoxic environment-induced high altitude pulmonary hypertension