四氯化碳诱导的肝硬化大鼠胰腺外分泌功能受损。

T Ogasawara, T Inagaki, T Yamada, H Ohara, T Nakazawa, M Itoh
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引用次数: 1

摘要

背景:大量研究表明慢性胰腺炎与肝硬化密切相关。然而,关于胰酶分泌的情况不太清楚。目的:探讨四氯化碳所致肝硬化大鼠胰腺外分泌功能的变化。方法:观察四氯化碳诱导肝硬化Sprague-Dawley大鼠胰腺外分泌功能及形态学变化。在离体胰腺腺泡中观察胆囊收缩素-8及其他分泌物刺激胰腺外分泌功能的变化,并通过常规组织学检查及电镜观察其体内及形态变化。结果:肝硬化大鼠的基础和胆囊收缩素-8刺激的腺泡淀粉酶释放量和腺泡淀粉酶含量明显低于对照组。在肝硬化大鼠中,没有一种分泌物能引起一定数量的淀粉酶释放。在体内,在基础和胆囊收缩素-8刺激条件下,胰液体积、淀粉酶和蛋白质产量显著降低。电镜显示肝硬化大鼠大部分粗面内质网伴少量核糖体扩张,部分线粒体肿胀。结论:胰腺外分泌功能在肝硬化大鼠中由于电子显微镜水平的改变而下降,反映了腺泡细胞内信使系统的受损。
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Impaired pancreatic exocrine function in rats with carbon tetrachloride-induced liver cirrhosis.

Background: Substantial numbers of studies have revealed the close correlation between chronic pancreatitis and cirrhosis in human. However, the situation with regard to pancreatic enzyme secretion is less clear.

Aim: The aim of the study was to investigate pancreatic exocrine function in rats with carbon tetrachloride-induced liver cirrhosis in rats.

Methods: Pancreatic exocrine function and morphology in Sprague-Dawley rats with carbon tetrachloride-induced liver cirrhosis were investigated. Pancreatic exocrine functions stimulated by cholecystokinin-8 and other secretagogs were assessed in isolated pancreatic acini, and in vivo and morphological changes were studied by routine histological examination and electron microscopy.

Results: The basal and cholecystokinin-8-stimulated amylase releases from acini and acinar amylase content were significantly lower in the cirrhotic rats than the control. None of the secretagogs induced the some amount of amylase release in cirrhotic as in control rats. Volume of the pancreatic juice and outputs of amylase and protein were significantly decreased under basal and cholecystokinin-8-stimulated conditions in vivo. Electron microscopy revealed most of the rough-surfaced endoplasmic reticulum accompanying less numbers of ribosomes to be dilated and some mitochondria to be swollen in cirrhotic rats.

Conclusion: Pancreatic exocrine functions are decreased in cirrhotic rats owing to alterations at the electron microscopic levels, reflecting an impaired acinar intracellular messenger system.

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