Koop I, Koop H, Gerhardt C, Schafmayer A, Arnold R
Dept. of Internal Medicine, University of Marburg, FRG.
Scand J Gastroenterol. 1989 Apr;24(3):315-20. doi: 10.3109/00365528909093053.
The influence of intraduodenal bile deficiency due to chronic bile duct obstruction and acute exogenous administration of bile acids on plasma cholecystokinin (CCK) and pancreatic polypeptide (PP) was investigated. Fourteen patients with tumor-induced bile duct stenosis and five healthy volunteers were given a liquid test meal. Four of the patients had a simultaneous pancreatic duct stenosis. On another day 4 g chenodeoxycholic acid were administered concomitantly with the liquid test meal in six of the patients and all controls. Basal and meal-stimulated plasma CCK did not differ between patients and controls. A pancreatic duct stenosis, which was associated with diminished plasma PP concentrations, had no influence on plasma CCK release. Exogenous bile acids significantly reduced the postprandial CCK response in both groups. Bile-induced inhibition was significantly greater in patients than in controls (75 +/- 7% and 44 +/- 11%, respectively; p less than 0.05). It is concluded that intraduodenal bile is an important modulator of the postprandial secretory activity of the CCK cell. Although chronic intraduodenal bile acid reduction in tumor-induced biliary duct stenosis did not influence plasma CCK levels, a negative feedback control of plasma CCK by acute bile acid administration could be demonstrated.
研究了慢性胆管梗阻导致的十二指肠内胆汁缺乏以及急性外源性给予胆汁酸对血浆胆囊收缩素（CCK）和胰多肽（PP）的影响。对14例肿瘤性胆管狭窄患者和5名健康志愿者给予流质试验餐。其中4例患者同时存在胰管狭窄。在另一天，6例患者和所有对照组在给予流质试验餐的同时给予4g鹅去氧胆酸。患者和对照组之间基础状态及餐后刺激的血浆CCK无差异。与血浆PP浓度降低相关的胰管狭窄对血浆CCK释放无影响。外源性胆汁酸显著降低了两组的餐后CCK反应。胆汁诱导的抑制作用在患者中显著大于对照组（分别为75±7%和44±11%；p<0.05）。结论是十二指肠内胆汁是CCK细胞餐后分泌活性的重要调节因子。虽然肿瘤性胆管狭窄导致的十二指肠内胆汁酸长期减少不影响血浆CCK水平，但急性给予胆汁酸可证明对血浆CCK存在负反馈控制。
