上海交通大学学报（医学版）

›› 2011, Vol. 31 ›› Issue (2): 165-.doi: 10.3969/j.issn.1674-8115.2011.02.010

• 论著（基础研究） • 上一篇    下一篇

丙泊酚对离体大鼠胸主动脉环的舒张作用

温翔宇1,2, 崔永耀3, 江 伟2, 王 莉2   

  1. 1.苏州大学研究生部, 苏州 215006；2.上海交通大学附属第六人民医院麻醉科, 上海 200233；3.上海交通大学 基础医学院药理学教研室, 上海 200025
  • 出版日期:2011-02-28 发布日期:2011-03-01
  • 通讯作者: 王 莉, 电子信箱: liwang1118@hotmail.com。
  • 作者简介:温翔宇（1983—）, 女, 硕士生；电子信箱: wxyzhjh@126.com。
  • 基金资助:

    国家自然科学基金（30972842）；上海市自然科学基金（09ZR1424000）

Vasodilation effect of propofol on isolated rat thoracic aorta rings

WEN Xiang-yu1,2, CUI Yong-yao3, JIANG Wei2, WANG Li2   

  1. 1.Department of Postgraduate, Soochow University, Suzhou 215006, China；2.Department of Anesthesiology, The Sixth People's Hospital, Shanghai Jiaotong University, Shanghai 200233, China；3.Department of Pharmacology, Basic Medical College, Shanghai Jiaotong University, Shanghai 200025, China
  • Online:2011-02-28 Published:2011-03-01
  • Supported by:

    National Natural Science Foundation of China, 30972842；Shanghai Natural Science Foundation, 09ZR1424000

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摘要：

目的 探讨丙泊酚对离体SD大鼠胸主动脉环的作用及可能机制。方法 将血管环随机分为内皮完整组和去内皮组，每组分别包括10-6 mol/L去甲肾上腺素（NA）处理组（n=6）、10-6 mol/L NA+丙泊酚处理组（n=6）、10-6 mol/L NA+0.18%脂肪乳剂（相当于10-4 mol/L丙泊酚中所含脂肪乳的量）处理组（n=6）、10-6 mol/L NA+10-4 mol/L丙泊酚处理组（n=6）、10-5 mol/L格列本脲（Gliben）+10-6 mol/L NA+丙泊酚处理组（n=6）、10-4 mol/L左旋硝基精氨酸甲酯（L-NAME）+10-6 mol/L NA+丙泊酚处理组（n=6）（去内皮组无此组）。10-6 mol/L NA收缩大鼠血管环达峰值后，每15 min加递增浓度（10-6、5×10-6、10-5、5×10-5和10-4 mol/L）的丙泊酚，观察血管张力的变化。结果 丙泊酚引起的血管舒张幅度呈浓度依赖性，在内皮完整组更明显，舒张幅度分别为（11.28±1.51）%、（25.23±4.03）%、（44.08±4.49）%、（66.28±4.83）%及（74.59±4.78）%，与相同浓度药物处理的去内皮组相比差异有统计学意义（P<0.01）。与NA+丙泊酚处理组相比，一氧化氮合成酶抑制剂L-NAME（10-4 mol/L）预处理可降低丙泊酚的血管舒张幅度（P<0.01）；特异性KATP通道抑制剂Gliben预处理血管环可降低丙泊酚的血管舒张幅度，且使低浓度（10-6和5×10-6 mol/L）丙泊酚的血管舒张效应转为收缩。结论 丙泊酚的血管舒张作用有浓度和内皮依赖性。一氧化氮和KATP通道介导了药物内皮依赖性的血管舒张。

关键词: 丙泊酚, 胸主动脉, 血管舒张, 一氧化氮, KATP通道

Abstract:

Objective To investigate the effect of propofol on isolated rat thoracic aorta rings, and explore the possible mechanism. Methods Vascular rings were randomly divided into endothelium-intact group and endothelium-denuded group, and each group was then divided into 5 subgroups: 10-6 mol/L norepinephrine (NA) group (n=6), 10-6 mol/L NA+propofol group (n=6), 10-6 mol/L NA+0.18% intralipid group (n=6), 10-6 mol/L NA+10-4 mol/L propofol group(n=6), 10-5 mol/L glibenclamide+10-6 mol/L NA+propofol group (n=6), 10-4 mol/L L-NAME +10-6 mol/L NA+propofol group (n=6) (this subgroup was not included in endothelial-denuded group). On the basis of maximal vasoconstriction evoked by NA （10-6 mol/L）, propofol was added in progressively increasing cumulative concentrations（10-6, 5×10-6, 10-5, 5×10-5 and 10-4  mol/L）at a 15 minute interval, and the effect of propofol on artery was observed as vascular tone changed. Results Propofol induced vasorelaxation at a concentration-dependent manner, and the effect was most significant in endothelium-intact group, with the vasodilation extent of （11.28±1.51）%,（25.23±4.03）%,（44.08±4.49）%,（66.28±4.83）% and (74.59±4.78）%，respectively, which were significantly different from those in endothelium-denuded group with same management （P<0.01）. Propofol-induced vasodilation was inhibited by L-NAME (10-4 mol/L), a nitric oxide synthase inhibitor (P<0.01）, and was also suppressed by glibenclamide, a specific inhibitor of KATP channels in endothelium-intact aorta. In addition, the vasodilation induced by 10-6 mol/L and 5×10-6 mol/L propofol was reversed by glibenclamide. Conclusion Propofol causes vasodilation of isolated thoracic aorta rings in rats in endothelium-dependent and concentration-dependent manners，and nitric oxide and KATP channels can mediate drug-induced vasodilation.

Key words: propofol, thoracic aorta, vasodilation, nitric oxide, KATP channels