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目的:在急性分离的胆管括约肌(sphincterofOddi,SO)细胞上,观察高胆固醇血症对SO细胞内钙振荡的影响变化及其机制.方法:新西兰雌兔24只随机分成两组:对照组和高胆固醇血症模型组各12只,以fluo-4/AM荧光指示剂负载急性分离的SO细胞,应用激光共聚焦扫描显微镜检测细胞钙振荡的变化.结果:高胆固醇血症组兔的SO细胞钙荧光强度振荡的幅度为6.11±3.1,正常组兔为3.61±0.94.当加入硝苯地平及EDTA后试验组钙荧光强度振荡幅度减小到2.24±0.72,下降了64%.当加入thapsigargin后,模型组钙荧光强度振荡幅度减小到3.8±1.9,下降了38%.结论:高胆固醇兔L-型电压依赖钙通道异常开放通过CICR途径所致SO细胞[Ca2+]1代谢紊乱是钙振荡物理学特征改变的分子生物学基础.
OBJECTIVE: To observe the effect of hypercholesterolemia on calcium oscillations in SO cells and its mechanism in acutely isolated sphincter of Oddi (SO) cells.Methods: 24 New Zealand female rabbits were randomly divided into two groups: control group and high Cholesterol model group, 12 rats in each group, acutely isolated SO cells were loaded with fluo-4 / AM fluorescent indicator, and the change of calcium oscillation was detected by confocal laser scanning microscopy.Results: In the hypercholesterolemia group, The amplitude of fluorescence intensity oscillation was 6.11 ± 3.1, and that of normal group was 3.61 ± 0.94. After addition of nifedipine and EDTA, the amplitude of calcium oscillation in the experimental group decreased by 64% when it was 2.24 ± 0.72. When adding thapsigargin, The oscillation amplitude of calcium fluorescence intensity in model group decreased to 3.8 ± 1.9, decreased by 38% .Conclusion: L-type voltage-dependent calcium channel in hypercholesterolemic rabbits is abnormally open due to CICR pathway.The metabolic disorder of [Ca2 +] 1 in SO cells is calcium oscillation physics Changes in molecular biology features.