胃肠激素对发育大鼠哺乳、胃排空及胰蛋白酶含量的影响。

Journal of developmental physiology Pub Date : 1993-04-01
K Kisfalvi, F Hajnal, G Varga, M Papp
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引用次数: 0

摘要

未标记的:本研究旨在探讨胃肠激素如外源性s.c.c erulein(6微克/公斤体重)、分泌素(100微克/公斤体重)、bombesin(20微克/公斤体重,s.c.c)、CCK-8(10微克/公斤体重,i.p)、CCK- a受体拮抗剂l364,718(100微克/公斤体重,i.p)、释放内源性CCK的camostate (400 mg/kg体重/ s)以及camostate与阿托品(250微克/公斤体重)共给药对胃肠激素的影响。s.c)或l364,718 (1 mg/kg)影响10日龄大鼠幼崽乳头摄乳量、胃排空和胰蛋白酶排出量。盐水处理的幼崽作为对照。非禁食的Wistar大鼠雌雄仔鼠按窝伴顺序使用。哺乳时间分别为30 min和45 min。一只小狗只被使用过一次。吃完奶后,幼崽被斩首,它们的胃和胰腺被切除并称重。胃中食物含量以牛奶的摄入量来表示,并以饱胃减去空胃之差来表示。测定胰蛋白酶、蛋白含量、血浆CCK水平。外源性药物对胃内容物没有影响。所研究的肽减少,l364,718,而胰蛋白酶/蛋白比增加。与生理盐水相比,卡莫酸使胃内容物增加60%,使胰蛋白酶/蛋白比降低90%。阿托品或l364,718不能逆转卡莫酸酯对胃和胰腺的影响。结论:外源性和内源性CCK似乎不影响牛奶摄入量,但降低胰蛋白酶/蛋白比。然而,内源性CCK抑制胃排空。在观察哺乳期间,CCK-8和甘油三酯的应用使血浆CCK水平升高。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Influence of gastrointestinal (GI) hormones on suckling, gastric emptying and pancreatic trypsin content in the developing rat.

Unlabelled: Aim of this study was to investigate how gastrointestinal hormones such as exogenous s.c. caerulein (6 micrograms/kg body weight), secretin (100 U/kg body weight), bombesin (20 micrograms/kg body weight, s.c.), CCK-8 (10 micrograms/kg body weight, i.p.), the CCK-A receptor antagonist L 364,718 (100 micrograms/kg body weight, i.p.), camostate (400 mg/kg body weight per os) which releases endogenous CCK and the coadministration of camostate with atropin (250 micrograms/kg body weight, s.c) or L 364,718 (1 mg/kg) influence milk intake from nipples, gastric emptying, and discharge of pancreatic trypsin content in 10-day-old rat pups. Saline-treated pups served as controls. The non-fasting Wistar rat pups of both sexes were used in littermate order. The suckling lasted for 30 and 45 min, respectively. One pup was used only once. After suckling the pups were decapitated, their stomach and pancreas were removed and weighed. The gastric food content was regarded as intake of milk and expressed as difference between the filled minus empty stomach. Pancreatic trypsin and protein content, plasma CCK level were measured. The exogenous agents did not influence gastric content. The investigated peptides decreased, L 364,718, however, increased the pancreatic trypsin/protein ratio. Camostate increased gastric content by 60% and decreased pancreatic trypsin/protein ratio vs saline by 90%. The gastric and pancreatic effects of camostate were not reversed by atropine or L 364,718.

Conclusion: Exogenous and endogenous CCK seem not to influence milk intake while decrease pancreatic trypsin/protein ratio. However, endogenous CCK inhibit gastric emptying. The plasma CCK level was elevated due to the applied CCK-8 and camostate during the observed suckling period.

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