摘要
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
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.
出处
《中国药房》
CAS
CSCD
2002年第3期136-138,共3页
China Pharmacy
基金
国家自然科学基金资助项目 (30070796)
北京市自然科学基金资助项目 (7012021)
