目的 探讨丙泊酚的血管舒张作用与蛋白激酶C （PKC）不同亚型间的关系。方法 将SD大鼠胸主动脉环随机分为内皮完整组（n=36）和去内皮组（n=36），每组各分6个亚组：①10 nmol/L Go6976+1×10^-6 mol/L去甲肾上腺素（NA）+丙泊酚处理组（n=6）；②10 μmol/L Rottlerin+1×10^-6 mol/L NA+丙泊酚处理组（n=6）；③2 μmol/L PKCε-Pseudo（假底物）+1×10^-6 mol/L NA+丙泊酚处理组（n=6）；④2 μmol/L PKCθ-Pseudo+1×10^-6 mol/L NA+丙泊酚处理组（n=6）；⑤2 μmol/L PKCζ-Pseudo+1×10^-6 mol/L NA+丙泊酚处理组（n=6）；⑥1×10^-6 mol/L NA+丙泊酚处理组（对照组，n=6）。PKCα抑制剂Go6976，PKCδ抑制剂Rottlerin，PKCζ、θ和ε假底物孵育血管环30 min后，加1×10^-6 mol/L NA收缩血管环达峰值，每15 min加递增浓度的丙泊酚（1×10^-6、5×10^-6、1×10^-5、5×10^-5、1×10^-4 mol/L），观察血管张力的变化。结果 内皮完整时，Go6976、PKCε假底物和PKCθ假底物减小丙泊酚引起的血管舒张幅度，与内皮完整的对照组相比差异有统计学意义（P<0.05）； Rottlerin抑制丙泊酚的血管舒张效应，且在1×10^-6~5×10^-5 mol/L丙泊酚作用时将舒张效应转为收缩（P<0.05）。去内皮时，Rottlerin、PKCε假底物和PKCθ假底物分别增大相同浓度丙泊酚作用下的血管舒张幅度，与去内皮对照组相比差异有统计学意义（P<0.05）；Go6976和PKCζ假底物分别增大1×10^-5~1×10^-4 mol/L丙泊酚作用下的血管舒张幅度（P<0.05）。结论 PKCα、δ、ε、θ参与了内皮完整时丙泊酚引起的血管舒张。

Objective To investigate the relationship between propofol-induced vasodilation and different protein kinase C(PKC) isoforms. Methods Vascular rings of SD rats were randomly divided into endothelium-intact group (n=36) and endothelium-denuded group (n=36), and each group was divided into 6 subgroups: ①10 nmol/L Go6976+1×10^-6 mol/L norepinephrine (NA)+ propofol group (n=6)；②10 μmol/L Rottlerin+1×10^-6 mol/L NA+propofol group （n=6）；③ 2 μmol/L PKCε-Pseudo+1×10^-6 mol/L NA+ propofol group （n=6）；④2 μmol/L PKCθ-Pseudo+1×10^-6 mol/L NA+ propofol group（n=6）；⑤2 μmol/L PKCζ-Pseudo+1×10^-6 mol/L NA+ propofol group （n=6）；⑥1×10^-6 mol/L NA+ propofol group(control group, n=6). PKCα inhibitor Go6976, PKCδ inhibitor Rottlerin, PKCζ-Pseudo, PKCθ-Pseudo and PKCε-Pseudo were used to pretreat isolated thoracic aorta rings for 30 min. Then 1×10^-6 mol/L NA evoked a steady maximal vasoconstriction, propofol was added in progressively increasing cumulative concentrations at a 15 min interval (1×10^-6, 5×10^-6, 1×10^-5, 5×10^-5 and 1×10^-4 mol/L), and the changes of vascular tone were observed. Results In endothelium-intact group, compared with endothelium-intact group, Go6976, PKCε-Pseudo and PKCθ-Pseudo inhibited propofol-induced vasodilation （P<0.05). Rottlerin also inhibited propofol-induced vasodilation, and even reversed the effect (1×10^-6 to 5×10^-5 mol/L propofol)(P<0.05). In endothelium-denuded group, compared with endotheliumdenuded control group, Rottlerin, PKCθ-Pseudo and PKCε-Pseudo enhanced propofol-induced vasodilation (P<0.05), and Go6976 and PKCζ-Pseudo enhanced vasodilation induced by 1×10^-5 to 1×10^-4 mol/L propofol (P<0.05). Conclusion PKCα, PKCδ, PKCε and PKCθ involve in propofol-induced vasodilation in intact endothelium.