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作 者:程南生[1] 朱精强[1] 吴沙沙[1] 李宁[1] 张明义[1] 姚有贵[1] 刘嘉林[1] 林琦远[1] 肖路加[1]
机构地区:[1]华西医科大学附属第一医院普外科,成都610041
出 处:《普外基础与临床杂志》1997年第4期197-200,共4页
摘 要:对免胆道不全梗阻与感染致胆红素钙结石成石过程中脂蛋白,尤其是高密度脂蛋白(HDL)代谢全过程作了测定。结果:实验组与对照组相比,血清游离胆固醇及HDL3-胆固醇明显升高,而HDL2-胆固醇及HDL-胆固醇明显减少;血浆卵磷酯-胆固醇酸基转移酶(LCAT)活性及肝细胞膜HDL受体最大结合力明显下降;胆汁中甘氨胆酸、甘氨脱氧胆酸及总胆酸明显减少;而肝组织中总胆固醇、甘油三酯及磷脂则均无显著性差异。本实验结果提示:在胆道不全梗阻及感染致胆红素钙结石成石过程中,存在因LCAT活性不足所致的HDL合成减少及成熟障碍,并有肝细胞膜HDL受体结合力下降,由于胆固醇逆向转运过程紊乱,在其它致石因素共同作用下导致色素性胆石的发生。We determined the whole process of lipoprotein metabolism during the formation of gallstone in rabbitmodel of calcium bilirubinate cholangiolithiasis. The main results included: the concentrations of free cholesterol andHDL3-cholesterol obviously increased in all experimental geroups while HDL-cholesterol, HDL2-cholesterol decreased,the activities of lecithin-cholesterol acytransferase(LCAT)and the Bmax of HDL-receptor in hepatic cell centrations ofglycocholic acid, glycodeoxychdic acid and total bile acid in the bile decreased obviously in experimental groups, thelevels of LDL-cholestrol, vLDL-cholesterol in the serum and total cholesterol, triglyceride in the hepatic tissue were notsignificant differences in all groups.According to the above results,it may be concluded that:there were disorders ofreduced HDL biosynthesis and its mature process caused by decreasing of LCAT activity during the formation of thegallstones caused by the bile duct obstruction and infection. Meanwhile, the Bmax of the HDL-receptor of the hepaticcell membrane decreased. Therefore, there were disorders of reverse cholesterol transport in many aspects. These factorstogether with other lithogenic elements Probably promote the formation of the calcium bilirubinate gallstones.
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