胆囊收缩素是人类胃酸分泌和餐后胃泌素释放的负调节因子。

Cholecystokinin is a negative regulator of gastric acid secretion and postprandial release of gastrin in humans.

作者信息

Schmidt W E, Schenk S, Nustede R, Holst J J, Fölsch U R, Creutzfeldt W

机构信息

First Department of Medicine, Christian-Albrechts-University, Kiel, Germany.

出版信息

Gastroenterology. 1994 Dec;107(6):1610-20. doi: 10.1016/0016-5085(94)90799-4.

DOI:10.1016/0016-5085(94)90799-4

PMID:7958670

Abstract

BACKGROUND/AIMS: The role of cholecystokinin (CCK) in the regulation of gastric acid secretion is still controversial. This study examined the effect of the CCK-A receptor antagonist loxiglumide (lox) on gastrin- or CCK-induced gastric acid secretion and meal-stimulated plasma gastrin levels in a placebo-controlled study.

METHODS

Acid output was studied in eight subjects who received intravenously gastrin-17 (15, 30, and 60 pmol.kg-1.h-1); gastrin-17 plus lox; cholecystokinin octapeptide (CCK-8) (15, 30, and 60 pmol.kg-1.h-1); CCK-8 plus lox; or gastrin plus CCK-8. Sham feeding-induced acid output and meal-stimulated gastrin secretion were studied during lox infusion.

RESULTS

Gastrin-17 dose-dependently stimulated acid output to near-maximal levels. CCK-8 (15 pmol.kg-1.h-1) increased acid secretion 2.5-fold over basal; higher infusion rates had less or no effect. When combined with lox, CCK-8 produced a near-maximal acid response (6-fold over basal). CCK-8 together with gastrin-17 inhibited gastrin-induced acid output by 67%. Meal-stimulated plasma gastrin concentrations were elevated 3.2-fold, whereas sham feeding-induced acid secretion was not modified by lox.

CONCLUSIONS

Blockade of CCK-A receptors converts CCK-8 into a potent acid secretagogue and augments postprandial gastrin secretion. A CCK-mediated stimulation of paracrine somatostatin secretion from antral and fundic D cells represents a candidate mechanism for the inhibition of the parietal and gastrin cell in humans.

摘要

背景/目的：胆囊收缩素（CCK）在胃酸分泌调节中的作用仍存在争议。本研究在一项安慰剂对照研究中，检测了CCK-A受体拮抗剂洛西肽胺（lox）对胃泌素或CCK诱导的胃酸分泌以及进餐刺激的血浆胃泌素水平的影响。

方法

对8名受试者进行酸分泌研究，他们分别静脉输注胃泌素-17（15、30和60 pmol·kg⁻¹·h⁻¹）；胃泌素-17加lox；八肽胆囊收缩素（CCK-8）（15、30和60 pmol·kg⁻¹·h⁻¹）；CCK-8加lox；或胃泌素加CCK-8。在输注lox期间，研究假饲诱导的酸分泌和进餐刺激的胃泌素分泌。

结果

胃泌素-17剂量依赖性地刺激酸分泌至接近最大水平。CCK-8（15 pmol·kg⁻¹·h⁻¹）使酸分泌比基础水平增加2.5倍；更高的输注速率作用较小或无作用。与lox联合使用时，CCK-8产生接近最大的酸反应（比基础水平高6倍）。CCK-8与胃泌素-17一起可使胃泌素诱导的酸分泌减少67%。进餐刺激的血浆胃泌素浓度升高3.2倍，而假饲诱导的酸分泌不受lox影响。