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内源性胆囊收缩素不参与清醒犬消化间期胃肠及胆囊运动的调节。

Endogenous CCK is not involved in the regulation of interdigestive gastrointestinal and gallbladder motility in conscious dogs.

作者信息

Mizumoto A, Ueki S, Ohtawa M, Itoh Z

机构信息

Institute of Endocrinology, Gunma University, Maebashi, Japan.

出版信息

Regul Pept. 1992 Oct 13;41(3):249-56. doi: 10.1016/0167-0115(92)90118-e.

Abstract

In this study, we assessed whether endogenous CCK is involved in the regulation of interdigestive gastrointestinal and gallbladder motility in conscious dogs with force transducers chronically implanted in the gastric antrum, duodenum, jejunum and gallbladder. L364718 at a dose of 1.0 mg/kg was used as a specific and potent CCK receptor blocker, and its effect on spontaneous interdigestive motility and plasma motilin release were examined. Additionally, the contractile activity of exogenous synthetic canine motilin (20-100 ng/kg) with or without pretreatment with L364718 at a dose of 1.0 mg/kg was assessed. Whether the blocking effect of L364718 on CCK receptors was sufficient or not was verified by giving CCK-OP at a bolus dose of 10 ng/kg. As a result, cyclic changes in interdigestive motor activity and the plasma motilin concentration were not affected by pretreatment with L364718. L364718 also did not affect motilin-induced interdigestive contractile activity in the gastrointestinal tract and gallbladder. On the other hand, the effect of CCK-OP was completely abolished by pretreatment with L364718. It is concluded that endogenous CCK is not involved in the regulation of spontaneous and motilin-induced interdigestive contractions in the canine gastrointestinal tract and gallbladder.

摘要

在本研究中,我们评估了内源性胆囊收缩素(CCK)是否参与调节清醒犬的消化间期胃肠和胆囊运动。这些犬长期在胃窦、十二指肠、空肠和胆囊植入力传感器。使用剂量为1.0 mg/kg的L364718作为特异性强效CCK受体阻滞剂,并检测其对消化间期自发运动和血浆胃动素释放的影响。此外,评估了给予或未给予剂量为1.0 mg/kg的L364718预处理时,外源性合成犬胃动素(20 - 100 ng/kg)的收缩活性。通过给予10 ng/kg推注剂量的CCK-OP来验证L364718对CCK受体的阻断作用是否充分。结果,L364718预处理不影响消化间期运动活动和血浆胃动素浓度的周期性变化。L364718也不影响胃动素诱导的胃肠道和胆囊消化间期收缩活性。另一方面,L364718预处理完全消除了CCK-OP的作用。得出的结论是,内源性CCK不参与调节犬胃肠道和胆囊的自发及胃动素诱导的消化间期收缩。

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