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。

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.