Ohta H, Guan D, Tawil T, Liddle R A, Green G M
Department of Physiology, University of Texas Health Science Center, San Antonio.
Gastroenterology. 1990 Sep;99(3):819-25. doi: 10.1016/0016-5085(90)90974-6.
To determine whether intraduodenal bile acids inhibit pancreatic secretion and cholecystokinin (CCK) release independent of pancreatic proteases, experiments were conducted in rats with bile and pancreatic juice chronically diverted to the ileum. Diversion of bile and pancreatic juice increased plasma CCK concentration to 19.1 +/- 4.0 pmol/L. Intraduodenal sodium taurocholate (78 mumol/h) reduced plasma CCK concentration to 6.6 +/- 1.5 pmol/L after 1 hour, but values increased to 17.3 +/- 2.3 pmol/L after 13.5 hours despite continued taurocholate infusion. Pancreatic protein secretion was also significantly but transiently inhibited by taurocholate. However, neither acute nor chronic intraduodenal bile infusion significantly reduced plasma CCK concentration compared with sodium bicarbonate infusion (13.4 +/- 1.9 pmol/L vs. 15.0 +/- 1.7 pmol/L, respectively). Chronic (13.5 hours) intraduodenal infusion of taurocholate plus pancreatic juice caused a sustained reduction of plasma CCK level to 3.1 +/- 0.5 pmol/L, which significantly increased to 9.4 +/- 1.1 pmol/L after cessation of taurocholate but with continued infusion of pancreatic juice. The results indicate that bile does not inhibit CCK release and that bile acids do not physiologically inhibit pancreatic secretion or CCK release independent of the presence of pancreatic proteases.
为了确定十二指肠内胆汁酸是否独立于胰腺蛋白酶而抑制胰腺分泌和胆囊收缩素(CCK)释放,在大鼠身上进行了实验,将胆汁和胰液长期引流至回肠。胆汁和胰液的引流使血浆CCK浓度升高至19.1±4.0 pmol/L。十二指肠内注入牛磺胆酸钠(78 μmol/h)1小时后,血浆CCK浓度降至6.6±1.5 pmol/L,但尽管持续注入牛磺胆酸钠,13.5小时后该值升至17.3±2.3 pmol/L。牛磺胆酸钠也显著但短暂地抑制了胰腺蛋白质分泌。然而,与注入碳酸氢钠相比(分别为13.4±1.9 pmol/L和15.0±1.7 pmol/L),十二指肠内急性或慢性注入胆汁均未显著降低血浆CCK浓度。十二指肠内慢性(13.5小时)注入牛磺胆酸钠加胰液使血浆CCK水平持续降至3.1±0.5 pmol/L,在停止注入牛磺胆酸钠但继续注入胰液后,该值显著升至9.4±1.1 pmol/L。结果表明,胆汁不抑制CCK释放,且胆汁酸在生理上不独立于胰腺蛋白酶的存在而抑制胰腺分泌或CCK释放。