肺动脉高压(pH)是高原心脏病主要病因,其严重程度亦决定该疾病的转归。慢性高原性pH的主要病理机制是低压性缺氧所致肺血管收缩及重构。肺动脉重构是各种pH进展的共同病理环节,阻遏或逆转肺动脉重构应成为治疗pH的标靶。本文拟通过观察辛伐他汀对大鼠在模拟5000m海拔高原的低压 Pulmonary hypertension (pH) is the main cause of high altitude heart disease, the severity also determines the outcome of the disease. The main pathogenesis of chronic high altitude pH is pulmonary vasoconstriction and remodeling induced by hypobaric hypoxia. Pulmonary remodeling is a common pathological link in the development of various pHs. Suppressing or reversing pulmonary remodeling should become the target for the treatment of pH. This article intends to observe the simvastatin on rats in simulating low altitude 5000m altitude