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采用兔胆红素结石模型，测定在胆道梗阻与感染胆红素钙结石成石过程中，肝组织脂质含量及肝细胞膜高密度脂蛋白（ＨＤＬ）受体的变化。结果发现：肝细胞膜ＨＤＬ受体Ｂ＿（ｍａｘｄ）于１周时胆道梗阻（ＢＯ）及胆道梗阻感染（ＢＯＩ）组即已降低，与对照组比较差异显著，分别为对照组的６９．０９％和４９．０９％（Ｐ＜０．０１）。６周时，ＢＯ和ＢＯＩ组分别维持在１周时水平。Ｋｄ值１周时ＢＯ和ＢＯＩ组与对照组无差异（Ｐ＞０．０５），至６周时，ＢＯ和ＢＯＩ组均明显高于对照组（Ｐ＜０．０５）。肝组织游离胆固醇各实验组均较对组照减少（Ｐ＜０．０１）。我们认为：在胆道梗阻与感染条件下，肝细胞膜ＨＤＬ受体功能存在异常，早期主要是受体数目减少，后期存在亲和力降低。因受体功能障碍，使肝细胞摄取ＨＤＬ减少，从而减少了用于胆汁酸合成的游离胆固醇量。可能最终引起胆汁酸合成减少，促进色素性结石的形成。
The rabbit bilirubin stone model was used to determine the changes of lipid content and HDL receptor in hepatic tissue during biliary obstruction and bilirubin calcium stone formation. The results showed that the maximal B HDL of hepatocyte membrane decreased at 1 week after biliary obstruction (BO) and biliary obstruction (BOI) group, which was significantly different from the control group (69.09% and 49.09% (P <0.01). At 6 weeks, the levels of BO and BOI were maintained at 1 week. There was no difference between BO and BOI group and control group at 1 week (P> 0.05). At 6 weeks, BO and BOI groups were significantly higher than those in control group (P <0.05). Liver free cholesterol in each experimental group than the control group decreased (P <0.01). We think: Under the conditions of biliary obstruction and infection, there are abnormalities of HDL receptor function in liver cell membrane. In the early stage, the number of receptors mainly decreases and the affinity decreases later. Due to receptor dysfunction, HDL uptake by hepatocytes is reduced, thereby reducing the amount of free cholesterol used for bile acid synthesis. May eventually lead to reduced bile acid synthesis, and promote the formation of pigmented stones.