Alcoholic pancreatic injury: alterations of pancreatic autonomic nerves and microcirculation.

H Ishii, M Nakamura, T Ito, S Nagata
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Abstract

Alteration of microcirculatory status and aberration of the autonomic nervous activity are thought to play an important role in the pathogenesis of ethanol-induced organ damages. Recently, the significant roles of nitric oxide and endothelin in the regulation of the pancreatic microcirculatory system and its disturbances have also been discovered. The present study was undertaken to clarify the histochemical and biochemical alteration of the cholinergic and adrenergic nerves. NADPH diaphorase and nitric oxide synthase activities, markers of nitroxergic nerves, and endothelin immunoreactivity as well as binding sites of 125 I-endothelin, were also studied in the pancreas of rats fed for three months with the Lieber-DeCarli's ethanol-containing liquid diet. In the rats fed ethanol, the histochemical and biochemical activities of the cholinergic nerves gradually increased, compared with the control rats. Monoamine fluorescence and NADPH diaphorase histochemical activity were also markedly enhanced in the ethanol-treated group. The results suggest that the activation of cholinergic and adrenergic nerves and increased NO synthesis are involved in the pathogenesis of ethanol-induced pancreatic injury.

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酒精性胰腺损伤:胰腺自主神经和微循环的改变。
微循环状态的改变和自主神经活动的异常被认为在酒精性器官损伤的发病机制中起重要作用。近年来,一氧化氮和内皮素在调节胰腺微循环系统及其紊乱中的重要作用也被发现。本研究旨在阐明胆碱能神经和肾上腺素能神经的组织化学和生化变化。用Lieber-DeCarli's含乙醇液体饲料喂养3个月的大鼠胰腺,研究了NADPH脱氢酶和一氧化氮合酶活性、氮能神经标志物、内皮素免疫反应性以及125 i -内皮素的结合位点。饲喂乙醇后,大鼠胆碱能神经的组织化学和生化活性较对照组逐渐升高。乙醇处理组单胺荧光和NADPH脱氢酶组织化学活性也显著增强。提示胆碱能神经和肾上腺素能神经的激活以及一氧化氮合成的增加参与了乙醇性胰腺损伤的发病机制。
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