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胆囊收缩素对人体胃酸分泌及胃排空的抑制作用。

Cholecystokinin in the inhibition of gastric secretion and gastric emptying in humans.

作者信息

Konturek S J, Kwiecien N, Obtulowicz W, Kopp B, Oleksy J, Rovati L

机构信息

Institute of Physiology, Academy of Medicine, Krakow, Poland.

出版信息

Digestion. 1990;45(1):1-8. doi: 10.1159/000200218.

DOI:10.1159/000200218
PMID:2340960
Abstract

Cholecystokinin (CCK) is known to inhibit gastric acid secretion and gastric emptying but its physiological role in the inhibition of gastric functions is not settled. In this study performed on 16 young male subjects, gastric acid secretion and emptying rate were determined after intragastric administration of 8% peptone meal alone or in combination with intravenous infusion of graded doses of CCK-8 (5-80 pmol/kg.h) or with addition of vegetable oil to meal without or with pretreatment with loxiglumide, a specific CCK antagonist. CCK-8 infusion at lower dose (5 pmol/kg.h) was ineffective but at higher doses (20-80 pmol/kg.h) it resulted in a significant reduction in acid output by 39 and 43% and a decrease in gastric emptying from 54% to 40 and 22%, respectively. Pretreatment with loxiglumide abolished almost completely the inhibition of both gastric acid and gastric emptying by CCK-8. Fat added to peptone meal reduced gastric acid secretion by 42-65% and decreased gastric emptying to 24-32%. The pretreatment with loxiglumide tended to reduce fat-induced inhibition of gastric acid secretion and gastric emptying but the difference in the inhibition of gastric functions between the tests without and with loxiglumide was not significant. This study provides evidence that exogenous CCK administered at pharmacological doses is a potent inhibitor of gastric acid secretion and gastric emptying and probably acts via specific CCK receptors. In contrast, fat induces inhibition of gastric acid secretion and gastric emptying that cannot be fully attributed to hormonally acting CCK.

摘要

已知胆囊收缩素(CCK)可抑制胃酸分泌和胃排空,但其在抑制胃功能方面的生理作用尚未明确。在这项针对16名年轻男性受试者进行的研究中,分别测定了单独给予8%蛋白胨餐、联合静脉输注不同剂量(5 - 80 pmol/kg·h)的CCK - 8或在餐食中添加植物油(有无特异性CCK拮抗剂洛西格列肽预处理)后胃酸分泌和排空率的变化。低剂量(5 pmol/kg·h)的CCK - 8输注无效,但高剂量(20 - 80 pmol/kg·h)时可使胃酸分泌显著减少39%和43%,胃排空率分别从54%降至40%和22%。洛西格列肽预处理几乎完全消除了CCK - 8对胃酸和胃排空的抑制作用。添加到蛋白胨餐中的脂肪使胃酸分泌减少42% - 65%,胃排空率降至24% - 32%。洛西格列肽预处理倾向于减轻脂肪对胃酸分泌和胃排空的抑制作用,但有无洛西格列肽预处理的试验在胃功能抑制方面的差异不显著。本研究提供了证据表明,以药理剂量给予的外源性CCK是胃酸分泌和胃排空的有效抑制剂,可能通过特异性CCK受体发挥作用。相比之下,脂肪引起的胃酸分泌和胃排空抑制不能完全归因于具有激素作用的CCK。

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Lack of endogenous cholecystokinin promotes cholelithogenesis in mice.
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Neurogastroenterol Motil. 2016 Mar;28(3):364-75. doi: 10.1111/nmo.12734. Epub 2015 Nov 25.
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Gastric motility following ingestion of a solid meal in a cohort of adult asthmatics.成人哮喘患者固体餐后胃动力。
J Neurogastroenterol Motil. 2013 Jul;19(3):355-65. doi: 10.5056/jnm.2013.19.3.355. Epub 2013 Jul 8.
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