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大鼠胰管阻塞后血浆和十二指肠胆囊收缩素浓度的变化

Changes in plasma and duodenal cholecystokinin concentrations after pancreatic duct occlusion in rats.

作者信息

Miyasaka K, Funakoshi A, Jimi A, Nakamura R, Matsumoto M, Kitani K

机构信息

Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology, Japan.

出版信息

Dig Dis Sci. 1992 Mar;37(3):369-77. doi: 10.1007/BF01307730.

Abstract

The changes in plasma and duodenal cholecystokinin (CCK) concentrations after pancreatic duct occlusion were examined in rats. The rats were sacrificed 1, 3, 7, 10, 14, and 30 days after occlusion of the duct. Histological examination showed acute inflammation on days 1 and 3 after duct occlusion, interstitial fibrosis and regenerative changes on days 7, 10, and 14, and pancreatic atrophy on day 30. The plasma CCK concentration increased from 0.45 pM to 2.0 pM after the occlusion and then remained high throughout the observation period. In contrast to the stable increase in plasma CCK concentration, the CCK content in the duodenum increased on days 1 and 3, decreased on day 7, increased on day 10, reaching over the control level on day 14, and then returned to the control level on day 30. Administration of boiled and 10-fold concentrated rat pancreatic juice or human pancreatic secretory trypsin inhibitor for seven days after pancreatic duct occlusion reversed the decrease in duodenal CCK content. The major molecular forms of duodenal CCK were CCK-8, -33, and -58. These results indicate that (1) basal plasma CCK concentration did not reflect the duodenal CCK content, (2) duodenal CCK content was well correlated with a decrease in inflammation in the pancreas, and (3) a nonenzymatic component in the pancreatic juice reversed the decrease in duodenal CCK content and body weight caused by pancreatic duct occlusion.

摘要

在大鼠中研究了胰管阻塞后血浆和十二指肠胆囊收缩素(CCK)浓度的变化。在胰管阻塞后的第1、3、7、10、14和30天处死大鼠。组织学检查显示,胰管阻塞后第1天和第3天出现急性炎症,第7、10和14天出现间质纤维化和再生变化,第30天出现胰腺萎缩。阻塞后血浆CCK浓度从0.45 pM升高至2.0 pM,然后在整个观察期内保持高位。与血浆CCK浓度的稳定升高相反,十二指肠中的CCK含量在第1天和第3天增加,第7天减少,第10天增加,在第14天超过对照水平,然后在第30天恢复到对照水平。胰管阻塞后给予煮沸并浓缩10倍的大鼠胰液或人胰腺分泌性胰蛋白酶抑制剂7天,可逆转十二指肠CCK含量的降低。十二指肠CCK的主要分子形式为CCK-8、-33和-58。这些结果表明:(1)基础血浆CCK浓度不能反映十二指肠CCK含量;(2)十二指肠CCK含量与胰腺炎症的减轻密切相关;(3)胰液中的非酶成分可逆转胰管阻塞所致十二指肠CCK含量降低和体重减轻。

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