论文部分内容阅读
采用兔模型，测定兔在胆红素钙结石成石过程中全套血脂质以及胆汁中胆汁酸（ＢＡ）含量。结果发现：各实验组的血清高密度脂蛋白胆固醇及高密度脂蛋白２胆固醇均较对照组降低，除单纯胆道梗阻（ＢＯ）１周组外均有显著性差异（Ｐ＜０．０１）。血清游离胆固醇及高密度脂蛋白３胆固醇各组均显著高于对照组（Ｐ＜０．０１）。胆汁中总胆汁酸在梗阻感染（ＢＯＩ）１周组已明显减少并持续存在（Ｐ＜０．０５），６周时仅为对照组的２４．１９％。ＢＯ１周组胆汁中８Ａ已开始下降，但无统计学差异（Ｐ＞０．０５），至６周时仅为对照组的３０．８７％，降低显著（Ｐ＜０．０５）。以上结果表明：在胆道梗阻感染情况下，主要是高密度脂蛋白合成减少及成熟障碍，使肝细胞摄取并用于ＢＡ合成的高密度脂蛋白胆固醇减少，最终导致胆汁中ＢＡ含量下降。并在其他因素参与下共同导致色素性结石的形成。
Rabbit model was used to determine the level of bile acid (BA) in whole blood lipid and bile in rabbits with bilirubin calculi. The results showed that the levels of serum high-density lipoprotein cholesterol and high-density lipoprotein-2 cholesterol in the experimental groups were significantly lower than those in the control group, except for the group of 1 week biliary obstruction (BO) (P <0.01). Serum free cholesterol and high-density lipoprotein-3 cholesterol in each group were significantly higher than those in the control group (P <0.01). Total bile acid in bile decreased and persisted in the first week of obstructive infection (BOI) group (P <0.05), only 24.19% of the control group at 6 weeks. The level of 8A in bile of BO1 group began to decline, but there was no significant difference (P> 0.05). Only the 30.87% of the control group had no significant difference (P <0.05). The above results show that in the case of biliary obstruction infection, the decrease of high density lipoprotein synthesis and the maturation are mainly caused by the reduction of high density lipoprotein cholesterol taken up by hepatocytes and used for the synthesis of BA, leading to the decrease of BA content in bile. And other factors in the joint lead to the formation of pigmented stones.