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 investigate the role of cholecystokinin (CCK) in gastric dysrhythmia and its neuropathological mechanism. Methods Based on the method of establishing antrum plexus retrograde apheresis, we used enzyme histochemistry and immunocytochemistry to observe the changes of the cholinergic (Ach) nerve in the myenteric plexus of gastric antrum, Nitric oxide synthase (NOS) nerve and CCK nerve changes. Results Electrogastrogram, abnormal rhythm index and slow wave frequency coefficient of variation in model group and CCK group were significantly higher than those in normal group (P <0.01); NOS nerve in model group and CCK group were significantly increased, while Ach Nerve content decreased significantly (P <0.01). Conclusions Increased exogenous and endogenous CCK can induce gastric electrical abnormalities. CCK through the activation of NOS, resulting in gastric electrical rhythm disorders. Anorexia of CCK and NOS in the antrum of the gastric antrum increases abnormally, and neuroregeneration of Ach is one of the neuropathological mechanisms.