阿托品减轻大鼠脑缺血后再灌流损害机制的初步探讨

Atropine ameliorates neuronal damage induced by cerebral ischemia and reperfusion in rats f An approach to the mechanism

为探讨乙酰胆碱（acetylcholine，Ach）在神经元缺血性损害中的作用和机制，本实验观察了Ach能M受体拮抗剂阿托品对大鼠脑缺血后再灌流损害的影响。发现阿托品（25mg／kgbw，ip）可明显减轻大鼠前脑缺血后再灌流所致海马CA1区神经元迟发性损害，减小大鼠大脑中动脉阻塞后再灌流损害范围，而对局部皮质血流变化无影响。表明阿托品对缺血脑组织的保护作用不是由于改善了局部脑血流。提示Ach参与了神经元缺血性损害，与M受体介导的信号传递有关。

To investigate the role of Ach (acetylcholine) in the development of ischemic neuronal injury and to elucidate its mechanism, we observed the effect of atropine-the antagonist of the muscarinic cholinergic receptor-on the neuronal damage induced by cerebral ischemia and reperfusion in rats. It was discovered that atropine (25 mg/kg bw, ip) ameliorated obviously the CA1 neuronal damage induced by the forebrain ischemia and reperfusion and reduced the brain infarction volume resulted from the middle cerebral artery occlusion and reperfusion, but had no effect on the cortex regional blood flow. These results demonstrated the protective action of atropine against ischemic brain damage was not by improving the regional blood flow. The results suggested that Ach take part in the ischemic neuronal damage through the activation of the muscarinic receptors.