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合成人胆囊收缩素-33对犬胰腺血流的影响。

Effect of synthetic human cholecystokinin-33 on pancreatic blood flow in dogs.

作者信息

Doi R, Hosotani R, Inoue K, Kogire M, Sumi S, Fujii N, Yajima H, Rayford P L, Tobe T

机构信息

First Department of Surgery, Faculty of Medicine, Kyoto University, Japan.

出版信息

Pancreas. 1990 Sep;5(5):615-20. doi: 10.1097/00006676-199009000-00019.

Abstract

We have examined the effect of synthetic human cholecystokinin (CCK-33 and CCK-8) on pancreatic blood flow and protein output in anesthetized dogs. Human CCK-33 and CCK-8 increased pancreatic blood flow and protein output in a dose-related manner. There were no significant differences in increasing pancreatic blood flow between human CCK-33 and CCK-8, and increases in blood flow were closely related to the increase of the pancreatic enzyme secretion. L-364,718 (20 nmol/kg) caused a potent inhibition of CCK-stimulated pancreatic blood flow as well as protein output. The degree of inhibition by L-364,718 was dependent on the amount of CCK infused. This study demonstrates that increasing effect on pancreatic blood flow may be one of the biological actions of CCK mediated via CCK receptor. The CCK-33, one of longer molecular forms of CCK, is an important biological stimulator of pancreatic blood flow as well as of exocrine pancreatic secretion.

摘要

我们研究了合成的人胆囊收缩素(CCK - 33和CCK - 8)对麻醉犬胰腺血流和蛋白质输出的影响。人CCK - 33和CCK - 8以剂量相关的方式增加胰腺血流和蛋白质输出。人CCK - 33和CCK - 8在增加胰腺血流方面无显著差异,且血流增加与胰腺酶分泌的增加密切相关。L - 364,718(20 nmol/kg)可有效抑制CCK刺激的胰腺血流以及蛋白质输出。L - 364,718的抑制程度取决于注入的CCK量。本研究表明,对胰腺血流的增加作用可能是CCK通过CCK受体介导的生物学作用之一。CCK - 33是CCK分子形式较长的一种,是胰腺血流以及胰腺外分泌的重要生物刺激物。

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