非对称性二甲基精氨酸对人阻力血管EDVD的抑制作用

首都医科大学学报 ›› 2009, Vol. 30 ›› Issue (2): 121-125.

非对称性二甲基精氨酸对人阻力血管EDVD的抑制作用

张东亮, 廖华, 张莉, 刘文虎

首都医科大学附属北京友谊医院肾病内科

收稿日期:2009-01-18 修回日期:1900-01-01 出版日期:2009-04-21 发布日期:2009-04-21
通讯作者: 刘文虎

Inhibition of Endothelium-dependent Vasodilatation by Asymmetric Dimethyl Arginine in Human Resistance Vessels

ZHANG Dong-liang, LIAO Hua, ZHANG Li, LIU Wen-hu

Department of Nephrology, Beijing Friendship Hospital, Capital Medical University

Received:2009-01-18 Revised:1900-01-01 Online:2009-04-21 Published:2009-04-21

摘要/Abstract

摘要： 目的探讨非对称性二甲基精氨酸(ADMA)对人离体阻力血管环内皮依赖性舒张(endothelium-dependent vasodilatation,EDVD)的抑制作用。方法在血液透析患者行动-静脉内瘘成形术时留取桡动脉,制备血管环,用机械法去内皮并设立内皮存在组和内皮缺失组。应用离体血管张力记录仪观察2组血管环在不同质量浓度ADMA(10^-7 mol/L、10^-6 mol/L、10^-5 mol/L、10^-4 mol/L和10^-3 mol/L)作用下张力的变化。内皮存在组用10^-5 mol/L苯肾上腺素(phenylephrine,PE)引发血管环收缩,再用质量浓度为10^-5 mol/L的乙酰胆碱(ACh)引发EDVD,然后用不同质量浓度ADMA处理,观察ADMA在内皮存在情况下对ACh所引起EDVD的抑制作用。内皮缺失组用质量浓度为10^-5 mol/L的PE引发血管环收缩后,再用质量浓度为10^-7 mol/L的硝普钠(SNP)引发非内皮依赖性血管舒张(EIVD),然后用不同质量浓度ADMA处理,观察ADMA在内皮缺失情况下对SNP引起EIVD的抑制作用。结果内皮存在组用10^-5 mol/L的ACh处理可使67.10%±18.63%因PE(10^-5 mol/L)引起收缩的血管舒张, ADMA对ACh引起的EDVD呈浓度依赖性抑制作用,相对收缩幅度依次为EDVD幅度的7.32%±8.60%(10^-7 mol/L)、20.03%±13.49%(10^-6 mol/L)、29.93%±11.78%(10^-5 mol/L)、43.30%±11.29%(10^-4 mol/L)和80.21%±18.16%(10^-3 mol/L)。在内皮缺失组,ADMA对SNP引起的EIVD呈微弱的抑制作用,且不表现为浓度依赖性。相对收缩幅度为EIVD的2.76%±1.98%(10^-7 mol/L)、2.27%±1.82%(10^-6 mol/L)、3.38%±2.99%(10^-5 mol/L)、3.59%±3.66%(10^-4 mol/L)和4.16%±3.67%(10^-3 mol/L)。结论 ADMA可以有效地抑制ACh引发的EDVD反应,该抑制作用呈浓度依赖性和内皮依赖性。

关键词: 非对称性二甲基精氨酸, 内皮依赖性血管舒张, 桡动脉

Abstract: Objective To study the inhibitory effects of asymmetric dimethyl arginine(ADMA) on endothelium-dependent vasodilation(EDVD) of human radial arteries. Methods Vascular rings were obtained from patients under maintenance hemodialysis(MHD) during internal arteriovenous fistula operation. According to the conditions of the endothelium, the arteries were divided into two groups: the endothelium intact group, and the endothelium deprived group, in which the endothelium was extracted mechanically. The arteries were then mounted on wire myographs. Contraction of the arteries were invoked with 10^-5 mol/L phenylephrine(PE), while EDVD was caused by a dose of 10^-5 mol/L acetylcholine(ACh) for the endothelium intact group or 10^-7 mol/L sodium nitroprusside(SNP) for the endothelium deprived group. Different concentrations of ADMA(10^-7~10^-3 mol/L) were used to test its inhibitory effects on EDVE. Cumulative concentration-response curves were then constructed for AMDA. Results For the endothelium intact group, the dilatation reached 67.10%±18.63%, when the arteries were subjected to 10^-5 mol/L ACh after PE(10^-5 mol/L)treatment. The inhibitory effects of ADMA on ACh-invoked EDVD were concentration-dependent. The relative contraction rates according to the concentrations of ACh were 7.32%±8.60%(ACh 10^-7 mol/L), 20.03%±13.49%(ACh 10^-6 mol/L), 29.93%±11.78%(ACh 10^-5 mol/L), 43.30%±11.29%(ACh 10^-4 mol/L), 80.21%±18.16%(ACh 10^-3 mol/L). For the endothelium deprived group, ADMA had a weak inhibitory effect on the endothelium independent vasodilatation(EIVD) caused by SNP. There were no concentration-dependent changes according to the concentration of ADMA. Relative constriction rates were 2.76%±1.98%(ADMA 10^-7 mol/L), 2.27%±1.82%(ADMA 10^-6 mol/L), 3.38%±2.99%(ADMA 10^-5 mol/L), 3.59%±3.66%(ADMA 10^-4 mol/L), 4.16%±3.67%(ADMA 10^-3 mol/L). Conclusion The results suggest that ADMA can inhibit EDVD caused by ACh. This effect is ADMA concentration-dependent, and endothelium-dependent.

Key words: asymmetric dimethyl arginine, endothelium-dependent vasodilatation, radial artery

中图分类号:

R 692.5

张东亮;廖华;张莉;刘文虎. 非对称性二甲基精氨酸对人阻力血管EDVD的抑制作用[J]. 首都医科大学学报, 2009, 30(2): 121-125.

ZHANG Dong-liang;LIAO Hua;ZHANG Li;LIU Wen-hu. Inhibition of Endothelium-dependent Vasodilatation by Asymmetric Dimethyl Arginine in Human Resistance Vessels[J]. Journal of Capital Medical University, 2009, 30(2): 121-125.

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