›› 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

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