胆囊收缩素在胃电节律失常中的作用及其神经病理学机制  

Effect and neuropathological mechanism of cholecystokinin on development of electrogastric arrhythmia in rats

作　　者：陈代陆[1] 王振华[2] 夏正武[3] 

机构地区：[1]成都军区昆明总医院内四科,昆明650032 [2]第三军医大学西南医院消化科 [3]成都军区昆明总医院检验科,昆明650032

出　　处：《中华消化杂志》2001年第7期420-422,共3页Chinese Journal of Digestion

摘　　要：目的　探讨胆囊收缩素 (CCK)在胃电节律失常中的作用及其神经病理学机制。方法　在建立胃窦肌间神经丛铺片方法的基础上 ,用酶组织化学与免疫细胞化学方法 ,观察胃电节律失常大鼠胃窦肌间神经丛内胆碱能 (Ach)神经、一氧化氮合酶 (NOS)神经及CCK神经的变化。结果　模型组和CCK组大鼠均出现胃电节律失常 ,异常节律指数及慢波频率变异系数均显著高于正常组 (P <0 .0 1) ;模型组和CCK组NOS神经显著增加 ,Ach神经含量显著减少 (P <0 .0 1)。结论　外源性及内源性CCK增加 ,能诱发胃电节律失常。CCK通过激活NOS ,产生胃电节律失常。胃窦肌间神经丛神经中CCK及NOS神经含量异常增加 ,Ach神经减少是发生胃电节律失常的神经病理学机制之一。Objective To study effects of cholecystokinin (CCK) on occuring of electrogastric arrhythmias. Methods The contens of cholecystokinin (CCK) nerves, cholinergic (Ach) nerves and nitregic nervous (NOS) nerves in antral myenteric plexus were studied using histochemistry and immunocytochemistry. Results (1) The electrogastric dysrhythmias occurred in the model and CCK groups rats, the abnormal rhythm index and coefficent of variation (cv) of slow wave frequency were singnificantly increased compared with the control ( P <0.01); (2) The contents of nitrergic nerves of model and CCK groups were significantly decreased ( P <0.01). Conclusion (1) The increased release of CCK or exogenous CCK can induce electrogastric arrhythmia. (2) The effects of CCK nerves on gastric myoelectric activities are mediate by nitrergic nerves. (3) Increase of contents of nitrergic and CCK nerves in antral myenteric plexus, and decrease of contents of cholinergic nerves were mechanism of neuropathology on development of electrogastric arrhythmias in rat.

关 键 词：胃电节律失常 一氧化氮合酶神经 胆碱能神经 胆囊收缩素 肌间神经丛 消化系疾病 病理学机制 

分 类 号：R333.2[医药卫生—人体生理学]