Heuman R, Norrby S, Sjödahl R, Tiselius H G, Tagesson C
Scand J Gastroenterol. 1980;15(5):581-6. doi: 10.3109/00365528009182219.
The possible role of conjugated bile salts in the induction and mediation of acute aseptic cholecystitis has been assessed. Using an experimental model, we determined the passive permeability to fluorescently labelled dextran in the gallbladder wall when exposed to different bile salts, alone or together with lecithin. Both taurocholate (20 mM) and, in particular, taurodeoxycholate (20 mM) markedly increased the transmural passage of dextran, but this effect was inhibited by lecithin (50 mM). Bile from patients with cholesterol gallstones contained relatively more deoxycholates (19.4% +/- 8.6%) and less lecithin (35 +/- 20 mmol/l) than did bile from patients with uncomplicated gastric disease (14.1 +/- 6.0% deoxycholates and 53 +/- 26 mmol lecithin/l). Since deoxycholates are more inflammation-promoting than cholates in several systems, and lecithin is considered necessary for protection against the devastating effects of bile salts, these findings should not be overlooked in current hypotheses on the pathogenesis of acute calculous cholecystitis.
共轭胆汁盐在急性无菌性胆囊炎的诱发和介导过程中可能发挥的作用已得到评估。我们利用一个实验模型,测定了胆囊壁在单独暴露于不同胆汁盐或与卵磷脂共同暴露时,对荧光标记葡聚糖的被动通透性。牛磺胆酸盐(20 mM),特别是牛磺脱氧胆酸盐(20 mM),显著增加了葡聚糖的跨壁通过率,但这种效应被卵磷脂(50 mM)抑制。与无并发症胃病患者的胆汁(脱氧胆酸盐14.1%±6.0%,卵磷脂53±26 mmol/l)相比,胆固醇结石患者的胆汁中脱氧胆酸盐含量相对更高(19.4%±8.6%),而卵磷脂含量更低(35±20 mmol/l)。由于在多个系统中,脱氧胆酸盐比胆酸盐更易促进炎症,且卵磷脂被认为是抵御胆汁盐破坏性作用所必需的,因此在当前关于急性结石性胆囊炎发病机制的假说中,这些发现不应被忽视。