【摘要】 分别用ＴＴＣ染色和ＨＥ染色观察大鼠大脑中动脉闭塞后乙酰胆碱（ＡＣｈ） 和谷氨酸（Ｇｌｕ） 对梗塞面积及细胞形态的影响； 采用皮质脑电图记录方法， 观察大鼠双侧颈总动脉夹闭后， Ｇｌｕ、ＡＣｈ 及ＡＣｈ 受体激动剂、拮抗剂对脑电图恢复时间的影响。结果发现： Ｇｌｕ 可使梗塞面积扩大， ＡＣｈ 可使Ｇｌｕ 的这种效应放大３０％ （Ｐ＜ ０．０１）； 脑缺血后Ｇｌｕ 使缺血区细胞破坏加重，ＡＣｈ 可加剧细胞的崩解，Ｇｌｕ 致缺血性皮质神经元兴奋性存在量效关系，其阈值为１０－ ２ｍ ｏｌ／Ｌ， ＡＣｈ 可使之降为１０－ ３ ｍ ｏｌ／Ｌ， ＡＣｈ 的这种作用可被阿托品所阻断而不被六羟季胺拮抗， 可被氨甲酰胆碱呈浓度－ 效应模拟， 而不被烟碱模拟。可见， 脑缺血时， 乙酰胆碱通过Ｍ 型受体降低谷氨酸兴奋毒性的阈值而表现出加强谷氨酸的神经兴奋毒性作用。更多还原

【Abstract】 TTC staining and HE staining were used to observe the influence of acteylcholine (ACh) and glutamate (Glu) on infarction area and cell morphology after middle cerebral artery occlusion (MCAO) in rats, and electrocorticography (ECG) applied to investigate the influence of Glu, ACh, ACh receptor activator and ACh antagonist on restoring time of EEG during bilateral common carotid artery occlusion (CCAO) in rats. The results showed that Glu could enlarge the infart area, ACh magnified the effect of Glu about 30% ( P <0 01); Glu maked cell damage heavier in ischemic area after cerebral ischemia, ACh aggravated cell to destroy. Glu induced neocortex neuronal excitation in a dose effect manner. The threshold of neuronal excitotoxicity induced by Glu was 10 -2 mol/L, which could be lowered to 10 -3 mol/L by ACh. The effect of ACh could be antagonized by atropine, rather than by hexamethonium, simulated by carbachol in a concentration effect manner, rather than by nicotine. It was concluded that ACh potentiated glutamate induced neuronal excitotoxicity by way of m ACh R to lower Glu threshold.更多还原