中缝隐核对兔奥迪氏括约肌肌电活动的影响

实验用电生理学和微量注射法观察了兔中缝隐核（NRO）对奥迪氏括约肌肌电活动的影响,动物禁食但自由饭水,18－24h手用乌拉坦（1.0g/kg)静脉麻醉,用双极康铜丝电极引导奥迪氏括约肌肌电,发现NRO内微注射谷氨酸（340mmol/L,0.4ul)可使奥迪氏括约肌肌电活动加强,与在NRO内微量注射生理盐水或者将谷氨酸（340mmol/L,0.4ul)注射到NRO以外的地方相比,具有显著差异（P＜0．01）,NRO 微量注射N-methy-D-aspartate(NM-DA)受体阻断剂氯胺酮（180mmol/L,0.1ul),可消除谷氨酸的效应,而将微量非NMDA受体阻断剂CNQX（2mmol/L,0.1ul)注入NRO,可使奥迪氏括约肌肌电加强,外周应用M－受体阻断剂阿托品（0.2mg/kg)或双侧颈部迷走神经切断,可阻断微量谷氨酸注射到NRO内所引起的效应,静脉注射α－受体阻断剂酚妥拉明（1.5mg/kg),心得安（1.5mg/kg)或自T3－4处切断脊髓,对NRO内微量注射谷氨酸的效应没有影响,结果提示,NRO对奥迪氏括约肌运行有调节作用,其中谷氨酸主要通过NMDA受体兴雷奥迪氏括约肌肌电活动,其传出途径是迷走神经和外周M受体。

Effect of nucleus raphe obscurus on myoelectric activity of sphincter of Oddi in rabbits

The aim of the present study was to investigate the role of nucleus raphe obscurus (NRO) in regulating the motility of sphincter of Oddi (SO). After fasting about l8~24 h, the rabbits were anesthetized with urethane (1.0 g/kg), and the myoelectric signals of SO were induced by a pair of copper electrodes inserted into the subsera. The results of microinjection of various drugs into NRO are as follows. After glutamate (340 mmol/L, 0.1 microl) was injected, activity of SO was excited. With microinjection of GABA (1 mol/L,0.1 microl), the spike burst of SO was inhibited. Following microinjection of ketamine (180 mmol/L, 0.1 microl), a kind of N-methyl-D-aspartate (NMDA) receptor antagonist, SO motility was inhibited and the effect of glutamate was abolished. Injection of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) (2 mmol/L, 0.1 microl), a non-NMDA receptor antagonist, also excited the myoelectric activity of SO, but did not inhibit the effect of glutamate. The effect of glutamate was abolished by intravenous injection of atropine (0.2 mg/kg) or bilateral vagotomy, but not by injection of phentolamine (1.5 mg/kg) or propronalol (1.5 mg/kg), or by transection of the spinal cord. The above results indicate that NRO mediation of SO activity is due to the effect of glutamate on the NMDA receptors in the nucleus, the output of which is sent through vagal nerve and peripheral M cholinergic receptor to exert excitation of gallbladder motility.