Inhibition of gastric emptying is a physiological action of cholecystokinin.
Inhibition of gastric emptying is a physiological action of cholecystokinin.
复制标题
抑制胃排空是缩胆囊素的生理作用。
DOI：
10.1016/s0016-5085(75)80236-8
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发表时间：
1975
期刊：
影响因子：
29.4
通讯作者：
M. Grossman
中科院分区：
文献类型：
--
作者：
Haile T. Debas;Omar Farooq;M. Grossman
本研究旨在确定胆囊收缩素（CCK）是否在抑制胃排空中起生理作用。通过连续静脉输注而不是推注给予CCK，通过使用已知明显次最大胰腺蛋白分泌和胆囊收缩的剂量，以及通过释放内源性CCK来模拟生理条件。用0.15mNaCl溶液300 ml灌胃4只胃瘘犬，10 min后测定胃内液体残留量，测定胃排空率。在静脉输注生理盐水（对照）和不同剂量的98%纯CCK，药物可利用的20%纯CCK，合成的CCK的COOH-末端八肽（OP-CCK），五肽胃泌素和十七肽胃泌素期间，研究排空率。内源性释放的CCK的影响进行了研究，通过测量排空的解决方案，其中不同浓度的色氨酸取代等渗量的NaCl的速率。20%纯CCK（3U·kg ~（-1）·hr ~（-1））和OP-CCK（125 ng·kg ~（-1）·hr ~（-1））抑制胃排空的D_（50）与其促胆囊运动和促胰酶作用的D_（50）大致相同。相比之下，尽管五肽胃泌素和十七肽胃泌素都抑制胃排空，但该作用所需的剂量远高于刺激胃酸分泌所需的D50。OP-CCK的有效性表明，胃排空的抑制是由于CCK本身，而不是CCK制剂中的杂质。我们已经证实了这一点，直接表明，纯CCK是一种有效的胃排空抑制剂。色氨酸也抑制胃排空。在其他狗中，在色氨酸抑制胃排空的时间内，胰腺蛋白分泌和胆囊收缩被刺激。这一证据支持这样的观点，即抑制胃排空是CCK的生理作用之一，但在胃泌素的情况下，它必须被视为一种药理作用。
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 0.15mNaCl. 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-1hr-1) and of OP-CCK (125 ng kg-1hr-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.