高同型半胱氨酸血症诱导eNOS脱偶联损害冠状动脉内皮功能  

Homocysteine impairs coronary artery endothelial function by uncoupling endothelial nitric oxide synthase in patients with hyperhomocysteinemia

作　　者：王莹[1] 何立芸[2] 毛节明[2] 王广[2] 

机构地区：[1]北京市海淀医院,北京100080 [2]北京大学第三医院

出　　处：《山东医药》2011年第36期9-10,13,共3页Shandong Medical Journal

基　　金：国家自然科学基金资助项目(30770873;81070244);国家重点基础研究发展计划973资助项目(2011CB503904)

摘　　要：目的探讨高同型半胱氨酸血症(HHcy)患者冠状动脉内皮功能是否被损伤,以及这种损伤是否通过内皮型一氧化氮合酶(eNOS)脱偶联实现的。方法 71例参与者被分成健康对照组(n=50)和HHcy组(n=21),利用多普勒超声心动测定腺苷诱导下冠状动脉左前降支的舒张功能的改变,冠脉血流速度储备(CFVR)由最大血流速度与基线水平的比值计算得出。采用ELISA以及高效液相色谱法测定血浆一氧化氮(NO)、四氢生物蝶呤(BH4)的水平。结果与健康对照组相比,HHcy组患者血浆NO、BH4的水平降低(P<0.05);HHcy组CFVR低于健康对照组(P<0.05);血浆Hcy水平与NO及CFVR呈负相关(P<0.05)。结论 HHcy可能通过降低BH4生物利用度,诱导eNOS脱偶联,而导致冠状动脉内皮功能损伤,进而促进不良冠脉事件的发生。Objective To investigate whether coronary artery endothelial function was damaged in patients with chronic hyperhomocysteinemia（HHcy） and if so,whether this impaired endothelial function is induced by the uncoupling of endothelial nitric oxide synthase（eNOS）.Methods The 71 subjects were divided into 2 groups,control（n=50） and HHcy（n=21）.CFVR was measured by noninvasive Doppler echocardiography.Plasma levels of tetrahydrobiopterin（BH4） and nitric oxide（NO） were measured by high-performance liquid chromatography and ELISA kits,respectively.Results Plasma levels of NO and BH4 were significantly lower in patients with HHcy than in controls（P0.05）.CFVR was markedly reduced in the HHcy group than control group（P0.05）.In addition,plasma level of homocysteine was negatively correlated with NO and CFVR.Conclusion Our results showed that chronic HHcy may contribute to coronary artery disease by inducing dysfunction of the coronary artery endothelium through uncoupling of eNOS.

关 键 词：高同型半胱氨酸血症 冠状动脉内皮功能 一氧化氮 内皮型一氧化氮合酶 

分 类 号：R541.4[医药卫生—心血管疾病]