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清醒大鼠中胆汁与胰液改道对胆囊收缩素释放及胰腺的相互作用。

Interactions between bile and pancreatic juice diversions on cholecystokinin release and pancreas in conscious rats.

作者信息

Nakamura R, Miyasaka K, Funakoshi A, Kitani K

机构信息

First Department of Internal Medicine, Tokyo Medical and Dental University, Japan.

出版信息

Proc Soc Exp Biol Med. 1989 Nov;192(2):182-6. doi: 10.3181/00379727-192-42976.

Abstract

Pancreatic exocrine secretion in the conscious rat is regulated by proteases secreted by the pancreas, and cholecystokinin (CCK) is known to be involved in its mechanism. It has also been reported that the absence of either pancreatic juice or bile in the duodenum could stimulate pancreatic secretion. Therefore, differences in CCK release responding to the exclusion of bile, pancreatic juice (PJ), or both bile and pancreatic juice (BPJ) from the intestine were examined by using a bioassay for cholecystokinin. Plasma CCK levels were increased by all three treatments compared with the basal value, the order of their effects being BPJ greater than PJ greater than bile diversion, and CCK concentrations produced by BPJ diversion were much greater than can be explained as simply summed effect of exclusions of bile and PJ. Pancreatic exocrine secretions were significantly increased by PJ and BPJ diversions, but the effect of bile diversion on the pancreas was not statistically significant. An additional infusion of CR-1409 (0.1 mg/rat), one of CCK receptor antagonists, inhibited exocrine function stimulated by BPJ diversion. We conclude (i) BPJ diversion is the strongest endogenous stimulant on CCK release; (ii) the potentiation between bile and PJ diversions is induced on CCK release; (iii) pancreatic protein secretion during BPJ diversion is mainly modulated by CCK.

摘要

清醒大鼠的胰腺外分泌受胰腺分泌的蛋白酶调节,已知胆囊收缩素(CCK)参与其调节机制。也有报道称十二指肠中缺乏胰液或胆汁可刺激胰腺分泌。因此,通过使用胆囊收缩素生物测定法,研究了肠道中胆汁、胰液(PJ)或胆汁和胰液(BPJ)排除后CCK释放的差异。与基础值相比,所有三种处理均使血浆CCK水平升高,其作用顺序为BPJ大于PJ大于胆汁引流,且BPJ引流产生的CCK浓度远高于胆汁和PJ排除的简单相加效应所能解释的水平。PJ和BPJ引流显著增加胰腺外分泌,但胆汁引流对胰腺的作用无统计学意义。额外输注CCK受体拮抗剂之一的CR-1409(0.1mg/大鼠)可抑制BPJ引流刺激的外分泌功能。我们得出结论:(i)BPJ引流是CCK释放最强的内源性刺激物;(ii)胆汁和PJ引流之间对CCK释放存在协同增强作用;(iii)BPJ引流期间胰腺蛋白质分泌主要受CCK调节。

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