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目的研究兔胆道口括约肌(sphincter of Oddi,SO)平滑肌细胞在胆固醇脂质体作用后收缩性的变化,探讨高胆固醇血症兔SO 动力异常的机制方法取纯种新西兰兔 SO 段,用Ⅱ型胶原酶消化获得单个平滑肌细胞,与胆崮醇/卵磷脂摩尔比为2:1和0.5:1的胆固醇脂质体(1g/L)分别孵育2 h 后,用不同浓度 KCl(9-24)nmol/L,乙酰胆碱(10~(12)～10~(-6))mol/L 作用于平滑肌细胞,激动剂作用后30s,加入丙烯醛固定,分别测量各组细胞的收缩百分比.结果兔 SO 平滑肌细胞平均长度为(143.7±12.3)μm,经胆固醇脂质体作用后平均长度无明显变化,对 KCl 和乙酰胆碱呈浓度依赖性收缩.KCl(18mmol/L)诱导最大收缩比为22.2%±0.7%,而2:1的胆固醇脂质体作用后收缩比为16.5%±0.6%(P<0.01);乙酰胆碱(10~(-7)mol/L)诱导最大收缩比为20.3%±1.4%,2:1的胆固醇脂质体作用后收缩比为16.5%±1.3%(P<0.05).摩尔比为0.5:1胆固醇脂质体作用后最大收缩比分别为21.3%±1.4%和19.2%±1.1%,同对照组相比无显著下降.结论兔 SO 平滑肌细胞经摩尔比2:1的胆固醇脂质体后起收缩性下降,推测这是高胆固醇血症可以导致兔 SO 的动力异常的机制.
Objective To investigate the contractile changes of sphincter of Oddi (SO) smooth muscle cells after cholesterol liposomes and explore the mechanism of SO abnormality in hypercholesterolemic rabbits. After being incubated with cholesterol liposomes (1 g / L) with cholestanol / lecithin molar ratio of 2: 1 and 0.5: 1 respectively for 2 h after collagenase digestion, single smooth muscle cells were treated with different concentrations of KCl (9-24) (10 ~ (12) ~ 10 ~ (-6)) mol / L, respectively, and then acrolein was added to the smooth muscle cells 30 min after the agonist, and the percentage of cell contraction was measured respectively.Results Rabbit SO The average length of smooth muscle cells was (143.7 ± 12.3) μm, the average length of cholesterol smooth muscle cells did not change significantly, and KCl and acetylcholine contraction in a concentration dependent manner.KCl (18mmol / L) induced maximum contraction ratio of 22.2% ± 0.7 (P <0.01). The maximal contractility induced by acetylcholine (10 -7 mol / L) was 20.3% ± 1.4% after 2: 1 cholesterol liposomes treatment, Cholesterol liposomes with a ratio of 2: 1 had a contraction ratio of 16.5% ± 1.3% (P <0.05), a molar ratio of 0.5: 1 21.3% ± 1.4% and 19.2% ± 1.1%, respectively, which showed no significant decrease compared with the control group.Conclusion The rabbit VSMCs have a contractile decline after cholesterol liposomes with molar ratio of 2: 1, which is presumed to be the result of hypercholesterolemia Hyperlipidemia can result in a mechanism of abnormal motility of rabbit SO.