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电刺激小脑顶核对大鼠胃缺血- 再灌注损伤的神经调控

蒋信伟, 杜东书, 张建福, 张咏梅, 周晓燕, 马小波

徐州医学院 机能学实验室；生理学教研室； 神经生物学研究中心，徐州 221002

摘要

本实验采用夹闭大鼠腹腔动脉30 min后松开动脉夹血流复灌1 h的方法建立胃缺血-再灌注(gastric ischemia-reperfusion, GI-R)损伤模型，在此模型基础上观察电刺激小脑顶核(fastigial nucleus, FN)对大鼠GI-R 损伤的影响，并对其可能的神经调 控机制进行初步的探讨。胃黏膜损伤检测显示，电刺激小脑FN 使GI-R 损伤显著减轻，且有强度- 效应依赖关系；另外， 电刺激小脑FN 使胃黏膜细胞的凋亡率降低。预先化学损毁小脑FN，则可消除电刺激对GI-R 损伤的减轻作用。内脏大神 经放电检测分析显示，电刺激小脑FN 使内脏大神经放电频率减少和放电幅度降低，而化学损毁双侧下丘脑外侧区(lateral hypothalamic area, LHA)，再电刺激FN，内脏大神经的放电频率、幅度与刺激FN 前相比都无明显变化。剪断双侧内脏 大神经，再电刺激小脑FN，同样可使GI-R 损伤减轻。化学损毁双侧LHA 能取消电刺激小脑FN 对GI-R 损伤的减轻作用。 氧化应激方面，电刺激小脑FN 使缺血- 再灌注的胃黏膜内超氧化物歧化酶(SOD)活性升高、丙二醛(MDA)含量降低。以 上结果提示：电刺激小脑FN 对大鼠缺血- 再灌注的胃黏膜具有保护作用，小脑FN 可能是对大鼠GI-R 损伤具有调控作用的 中枢部位，其神经机制可能是通过LHA 介导，降低了交感神经的兴奋性实现的，此外可能还与其抗氧化作用有关。

关键词： 大鼠; 小脑顶核; 下丘脑外侧区; 胃缺血- 再灌注; 内脏大神经; 凋亡

分类号：Q426;Q482;R322.81

[The neuroregulatory effect of cerebellar fastigial nucleus stimulation on gastric ischemia-reperfusion injury in rats.] [Ariticle in Chinese]

JIANG Xin-Wei, DU Dong-Shu, ZHANG Jian-Fu, ZHANG Yong-Mei, ZHOU Xiao-Yan, 　　　　 MA Xiao-Bo

Laboratory of Functional Experiments； Department of Physiology； Research Center for Neurobiology, Xuzhou Medical College, Xuzhou 221002, China

Abstract

In the present study, rat model of gastric ischemia-reperfusion (GI-R) injury was established by clamping the celiac artery for 30 min followed by 1 h of reperfusion. Subsequently, the regulatory effect of electrical stimulation of cerebellar fastigial nucleus (FN) on GI-R injury and its neural mechanisms were investigated in Sprague-Dawley rats. The results are as follows. Electrical stimulation of the cerebellar FN not only obviously attenuated the GI-R injury in an intensity-dependent manner, but also decreased the apoptosis rate of gastric mucosal cells. Chemical lesion of FN eliminated the protective effect of electrical stimulation of FN on GI-R injury. Electrical stimulation of cerebellar FN decreased both the frequency and amplitude of the discharges of greater splanchnic nerve, but it could not change the discharge of greater splanchnic nerve following the lesion of the lateral hypothalamic area (LHA). After bilateral section of the greater splanchnic nerves, electrical stimulation of the FN also attenuated the GI-R injury. Chemical lesion of the LHA reversed the protective effect of electrical stimulation of FN on GI-R injury. Electrical stimulation of FN increased the activity of superoxide dismutase (SOD), but decreased the content of malondialdehyde (MDA) in gastric mucosa under GI-R. These results indicate that the cerebellar FN may regulate GI-R injury. Therefore, the cerebellar FN is an important brain site protecting the stomach against GI-R. The LHA and greater splanchnic nerves participate in the regulatory effects of cerebellar FN stimulation on GI-R injury. In addition, antioxidation may also be involved in the protection mechanism of cerebellar FN stimulation.

Key words: cerebellar fastigial nucleus; lateral hypothalamic area; gastric ischemia-reperfusion; greater splanchnic nerve; apoptosis; rat

收稿日期：2009-05-19　　录用日期：2009-08-04

通讯作者：张建福　　E-mail: jfzhang@xzmc.edu.cn

引用本文：

蒋信伟, 杜东书, 张建福, 张咏梅, 周晓燕, 马小波. 电刺激小脑顶核对大鼠胃缺血- 再灌注损伤的神经调控[J]. 生理学报 2009; 61 (5): 451-457.

JIANG Xin-Wei, DU Dong-Shu, ZHANG Jian-Fu, ZHANG Yong-Mei, ZHOU Xiao-Yan, 　　　　 MA Xiao-Bo . [The neuroregulatory effect of cerebellar fastigial nucleus stimulation on gastric ischemia-reperfusion injury in rats.] [Ariticle in Chinese] . Acta Physiol Sin 2009; 61 (5): 451-457 (in Chinese with English abstract).