Myers S I, Riva A, Kalley-Taylor B, Bartula L
Department of Surgery, University of Texas Southwestern Medical Center, Dallas.
Prostaglandins Leukot Essent Fatty Acids. 1995 Jan;52(1):35-9. doi: 10.1016/0952-3278(95)90094-2.
Rabbit common bile duct ligation has been shown to concomitantly increase levels of gallbladder taurodeoxycholic acid and gallbladder eicosanoid release. This study examines the hypothesis that taurodeoxycholic acid, a known chemical mediator of gallbladder inflammation, stimulates endogenous gallbladder eicosanoid release. Male New Zealand white rabbits were anesthetized, gallbladders removed and perfused in vitro with Krebs-Henseleit buffer (pH 7.4, 37 degrees C) at 1 ml/min with increasing doses of taurodeoxycholic acid (0, 10, 30 and 100 mM) added to the perfusate. The effluent was collected at 15, 30, 60 and 120 min of perfusion and assayed for 6-keto-PGF1 alpha (PGI2 metabolite), PGE2, and thromboxane B2 (TXB2) by enzyme immunoassay. Taurodeoxycholic acid increased gallbladder eicosanoid release in a dose-related manner with 6-keto-PGF1 alpha and PGE2 release 10-fold higher than TXB2. Indomethacin (1.5 mM) decreased gallbladder eicosanoid release by 50% in the gallbladders perfused with 30 mM taurodeoxycholic acid, demonstrating that the increased gallbladder eicosanoid release was due to de novo synthesis. These findings suggest that the increased release of gallbladder PGI2 and PGE2 described in animal models of cholecystitis may, in part, be related to increased gallbladder bile levels of taurodeoxycholic acid.
兔胆总管结扎已被证明会同时增加胆囊牛磺去氧胆酸水平和胆囊类花生酸释放。本研究检验了这样一个假设，即牛磺去氧胆酸（一种已知的胆囊炎症化学介质）会刺激内源性胆囊类花生酸释放。雄性新西兰白兔麻醉后，切除胆囊并在体外以1毫升/分钟的速度用克雷布斯-亨塞尔特缓冲液（pH 7.4，37摄氏度）灌注，灌注液中添加递增剂量的牛磺去氧胆酸（0、10、30和100毫摩尔）。在灌注15、30、60和120分钟时收集流出液，并通过酶免疫测定法检测6-酮-前列环素F1α（前列环素I2代谢物）、前列腺素E2和血栓素B2。牛磺去氧胆酸以剂量相关的方式增加胆囊类花生酸释放，6-酮-前列环素F1α和前列腺素E2的释放比血栓素B2高10倍。吲哚美辛（1.5毫摩尔）使灌注30毫摩尔牛磺去氧胆酸的胆囊中胆囊类花生酸释放减少50%，表明胆囊类花生酸释放增加是由于从头合成。这些发现表明，在胆囊炎动物模型中描述的胆囊前列环素I2和前列腺素E2释放增加可能部分与胆囊胆汁中牛磺去氧胆酸水平升高有关。
