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目的:研究全脑缺血时沙土鼠海马、纹状体和皮层谷氨酸、天冬氨酸、γ-氨基丁酸(GABA)、谷氨酰胺、甘氨酸和牛磺酸含量的变化及氯胺酮对上述氨基酸含量的影响.方法:采用结扎双侧颈总动脉的方法制备沙土鼠全脑缺血模型,应用HPLC和荧光检测器联用测定氨基酸的含量.结果:全脑缺血显著增加沙土鼠海马,纹状体和皮层的谷氨酸,天冬氨酸,谷氨酰胺,GABA,甘氨酸和牛磺酸含量;氯胺酮(120 mg/kg,ip)预处理能完全逆转缺血诱导的谷氨酸、天冬氨酸、甘氨酸和谷氨酰胺释放的增加,但不能完全逆转缺血诱导的GABA和牛磺酸释放增加.结论:脑缺血诱发的神经元损伤可能与其增加谷氨酸、天冬氨酸、甘氨酸、谷氨酰胺含量有关,而抑制性氨基酸GABA和牛磺酸释放增加则可能是机体一种重要的自身脑保护机制.氯胺酮逆转脑缺血诱导的兴奋性氨基酸释放增加可能是其抗兴奋性神经毒的生化基础.
Objective: To investigate the changes of glutamate, aspartate, glutamate, glycine and taurine in hippocampus, striatum and cortex of gerbils during global cerebral ischemia, Amino acids content.Methods: The gerbil global cerebral ischemia model was prepared by ligation of common carotid arteries of both sides, and the contents of amino acids were determined by HPLC and fluorescence detector.Results: The global cerebral ischemia increased the hippocampus, Glutamate, aspartate, glutamine, GABA, glycine and taurine content in the striatum and cortex; Ketamine (120 mg / kg, ip) preconditioning completely reversed ischemia- But not completely reverse the increase of ischemia-induced GABA and taurine release.Conclusion: Neuronal injury induced by cerebral ischemia may be related to the increase of glutamate, aspartate, Glycine, glutamine content, while the increase of inhibitory amino acids GABA and taurine release may be an important self-protection mechanism of the body.Ketamine reverses the increase of excitatory amino acid release induced by cerebral ischemia may be its anti-excitability The biochemical basis poison.