L-精氨酸治疗缺氧性肺动脉高压

目的 :探讨L -精氨酸 (L -Arg)干预缺氧性肺血管结构重建的机制。方法 :将18只Wistar大鼠采用随机设计分为对照组、缺氧组和缺氧 +L -Arg组 (共6个配伍组 )。以右心导管法测定肺动脉压力 ,并对大鼠肺组织标本进行显微结构观察和超微结构观察 ,同时以免疫组化方法分析肺动脉I型胶原表达。结果 :缺氧组大鼠肺动脉平均压 (mPAP)为 (2 7±0 3)kPa ,对照组为 (2 1±0 1)kPa ,两者比较 ,P<0 05。缺氧组大鼠肺血管显微及超微结构发生明显改变 ,有肺血管结构重建形成。然而 ,缺氧 +L -Arg组大鼠mPAP为 (2 2±0 2)kPa ,缺氧组为 (2 7±0 3)kPa ,两者比较 ,P<0 05。L -Arg缓解了缺氧性肺血管结构重建的形成。结论 :L -Arg 对缺氧性肺血管结构重建以及缺氧性肺动脉高压的形成有重要的调节作用

Treatment of Hypoxic Pulmonary Hypertension With L－ arginine

OBJECTIVE:To study the mechanism by which L-arginine regulates hypoxic pulmonary vascular structural remodeling.METHODS:Eighteen Wistar rats were randomly divided into control group,hypoxic group and hypoxic+L-arginine group.Pulmonary artery pressure was measured with right cardiac catheterization.Micro-structure and ultra-structure of pulmonary tissue were observed and collagen I expression was evaluated with immunohistochemistry.RESULTS:Mean pulmonary artery pressure(mPAP) was(2.7±0.3)kPa in hypoxic rats and(2.1±0.1)kPa in control rats(P<0.05).In hypoxic rats the pulmonary artery structure obviously changed and pulmonary artery vascular structural remodeling developed.However,L-arginine attenuated mPAP to(2.2±0.2)kPa in hypoxic+L-arginine group.CONCLUSION:L-arginine plays an important role in the regulation of hypoxic pulmonary vascular structural remodeling and pulmonary hypertension.