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抑制胃排空是胆囊收缩素的一种生理作用。

Inhibition of gastric emptying is a physiological action of cholecystokinin.

作者信息

Debas H T, Farooq O, Grossman M I

出版信息

Gastroenterology. 1975 May;68(5 Pt 1):1211-7.

PMID:1126597
Abstract

This study was designed to determine whether cholecystokinin (CCK) plays a physiological role in the inhibition of gastric emptying. Physiological conditions were simulated by giving CCK by continuous intravenous infusion rather than by bolus injection, by using doses known to be distinctly submaximal for pancreatic protein secretion, and for gallbladder contraction, and by releasing endogenous CCK. The rate of gastric emptying was determined in 4 dogs with gastric fistulas by measuring the volume of fluid remaining in the stomach 10 min after instillation of 300 ml of 0.15 M NaCl. Rate of emptying was studied during intravenous infusion of saline (control) and of different doses of 98% pure CCK, commerically available 20% pure CCK, synthetic COOH-terminal octapeptide of CCK (OP-CCK), pentagastrin, and heptadecapeptide gastrin. The effect of endogenously released CCK was studied by measuring the rate of emptying of solutions in which different concentrations of tryptophan replaced equiosmolar amounts of NaCl. The d50's of 20% pure CCK (3 U kg minus-1 hr minus-1) and of OP-CCK (125 ng kg minus-1 hr minus-1) for inhibition of gastric emptying were about the same as their D50's for cholecystokinetic and pancreozyminic actions. By contrast, although both pentagastrin and heptadecapeptide gastrin inhibited gastric emptying, the doses required for this action were much higher than the D50's required for stimulation of gastric acid secretion. The effectiveness of OP-CCK indicates that inhibition of gastric emptying is attributable to CCK itself and not to an impurity in the CCK preparation. We have confirmed this directly by showing that pure CCK is a potent inhibitor of gastric emptying. Tryptophan also inhibited gastric emptying. In other dogs pancreatic protein secretion and gallbladder contraction were shown to be stimulated during the time tryptophan was inhibiting gastric emptying. This evidence supports the view that inhibition of gastric emptying is one of the physiological actions of CCK, but in the case of gastrin it must be regarded as a pharmacological action.

摘要

本研究旨在确定胆囊收缩素(CCK)在抑制胃排空过程中是否发挥生理作用。通过持续静脉输注而非大剂量注射给予CCK来模拟生理条件,使用已知对胰腺蛋白分泌和胆囊收缩明显低于最大剂量的剂量,并释放内源性CCK。通过测量向4只具有胃瘘的狗胃内注入300 ml 0.15 M NaCl 10分钟后胃内剩余液体的体积,来测定胃排空速率。在静脉输注生理盐水(对照)以及不同剂量的98%纯CCK、市售20%纯CCK、CCK的合成羧基末端八肽(OP-CCK)、五肽胃泌素和十七肽胃泌素期间研究排空速率。通过测量不同浓度色氨酸替代等渗量NaCl的溶液的排空速率,研究内源性释放的CCK的作用。20%纯CCK(3 U·kg⁻¹·hr⁻¹)和OP-CCK(125 ng·kg⁻¹·hr⁻¹)抑制胃排空的半数有效剂量(d50)与其引起胆囊收缩和促胰酶分泌作用的半数有效剂量(D50)大致相同。相比之下,尽管五肽胃泌素和十七肽胃泌素均抑制胃排空,但该作用所需剂量远高于刺激胃酸分泌所需的D50。OP-CCK的有效性表明胃排空的抑制归因于CCK本身而非CCK制剂中的杂质。我们通过证明纯CCK是胃排空的有效抑制剂直接证实了这一点。色氨酸也抑制胃排空。在其他狗中,在色氨酸抑制胃排空期间,胰腺蛋白分泌和胆囊收缩被证明受到刺激。该证据支持以下观点:胃排空的抑制是CCK的生理作用之一,但就胃泌素而言,必须将其视为一种药理作用。

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