Ishii H, Nakamura M, Ito T, Nagata S
Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Alcohol Alcohol Suppl. 1994;2:369-75.
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.
微循环状态的改变和自主神经活动的异常被认为在乙醇诱导的器官损伤发病机制中起重要作用。最近,一氧化氮和内皮素在胰腺微循环系统调节及其紊乱中的重要作用也已被发现。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改变。还对用Lieber-DeCarli含乙醇液体饲料喂养三个月的大鼠胰腺中的NADPH黄递酶和一氧化氮合酶活性、硝能神经标志物、内皮素免疫反应性以及125I-内皮素结合位点进行了研究。与对照大鼠相比,在喂食乙醇的大鼠中,胆碱能神经的组织化学和生化活性逐渐增加。乙醇处理组的单胺荧光和NADPH黄递酶组织化学活性也明显增强。结果表明,胆碱能神经和肾上腺素能神经的激活以及一氧化氮合成增加参与了乙醇诱导的胰腺损伤发病机制。