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十二指肠内胆汁盐对人体胰胆系统对蛙皮素和胆囊收缩素反应的影响。

Effect of intraduodenal bile salt on pancreaticobiliary responses to bombesin and to cholecystokinin in humans.

作者信息

Thimister P W, Hopman W P, Tangerman A, Rosenbusch G, Willems H L, Jansen J B

机构信息

Department of Gastroenterology and Hepatology, University Hospital Nijmegen, Nijmegen, the Netherlands.

出版信息

Hepatology. 1998 Dec;28(6):1454-60. doi: 10.1002/hep.510280602.

Abstract

Bile salts modulate postprandial gallbladder emptying and pancreatic enzyme secretion, possibly by interfering with plasma cholecystokinin (CCK) responses. The regulatory role of bile salts in the absence of nutrients from the gut is poorly understood. Therefore, we studied the effect of intraduodenal sodium chenodeoxycholate on bombesin (BBS)- or CCK-stimulated plasma CCK levels, plasma pancreatic polypeptide levels, gallbladder motility, and pancreatic enzyme secretion. In a crossover design, saline without or with chenodeoxycholate was perfused intraduodenally for 3 hours in healthy volunteers. During the last hour, either BBS (n = 9) or CCK (n = 10) was infused intravenously. Chenodeoxycholate inhibited BBS-stimulated gallbladder emptying from 59% +/- 4% to 34% +/- 6% (P <.05) and intraduodenal bilirubin output from 41 +/- 9 to 21 +/- 5 micromol/h (P <.05), but it increased integrated plasma CCK levels from 157 +/- 19 to 184 +/- 19 pmol/L. 60 min (P =.01). Similarly, chenodeoxycholate administration inhibited gallbladder emptying and bilirubin output in response to intravenous CCK. Chenodeoxycholate also tended to reduce pancreatic polypeptide release and intraduodenal amylase output in response to intravenous BBS or CCK. It is concluded that intraduodenal chenodeoxycholate administration inhibits BBS- or CCK-stimulated gallbladder emptying, probably by diminishing target organ sensitivity to circulating CCK.

摘要

胆汁盐可能通过干扰血浆胆囊收缩素(CCK)反应来调节餐后胆囊排空和胰腺酶分泌。目前对肠道缺乏营养物质时胆汁盐的调节作用了解甚少。因此,我们研究了十二指肠内注入鹅去氧胆酸钠对蛙皮素(BBS)或CCK刺激的血浆CCK水平、血浆胰多肽水平、胆囊运动及胰腺酶分泌的影响。采用交叉设计,在健康志愿者十二指肠内灌注不含或含有鹅去氧胆酸钠的生理盐水3小时。在最后一小时,静脉注射BBS(n = 9)或CCK(n = 10)。鹅去氧胆酸钠将BBS刺激的胆囊排空率从59%±4%降至34%±6%(P<.05),十二指肠胆红素输出量从41±9降至21±5 μmol/h(P<.05),但使血浆CCK综合水平从157±19升至184±19 pmol/L(60分钟时,P =.01)。同样,给予鹅去氧胆酸钠可抑制静脉注射CCK后的胆囊排空和胆红素输出。鹅去氧胆酸钠还倾向于减少静脉注射BBS或CCK后的胰多肽释放及十二指肠淀粉酶输出。结论是,十二指肠内给予鹅去氧胆酸钠可抑制BBS或CCK刺激的胆囊排空,可能是通过降低靶器官对循环CCK的敏感性来实现的。

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