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目的 :研究全脑缺血时沙土鼠海马谷氨酸 (Glu)、天门冬氨酸 (Asp)、γ 氨基丁酸 (GABA)、谷氨酰胺 (Gln)、甘氨酸 (Gly)和牛磺酸 (Tau)含量的变化及三磷酸腺苷敏感性钾通道 (KATP)开放剂依普卡 (IPK)和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 :双侧颈动脉结扎 5min及再灌注 6 0min ,沙土鼠海马Glu、Asp含量分别增加 40 %和 80 % ,而且GABA、Gln、Gly和Tau也明显增加 ;IPK(1 0～ 4 0mg·kg-1,ip)和氯胺酮 (12 0mg·kg-1,ip)治疗能逆转缺血诱导的Glu、Asp、Gln和Gly释放的增加 ,但不能逆转缺血诱导的GABA和Tau释放的增加。结论 :全脑缺血诱发的神经元损伤可能与其增加Glu、Asp、Gln和Gly含量有关 ,而抑制性氨基酸GABA和Tau释放增加则可能是机体一种重要的自身脑保护机制。IPK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 effects of global cerebral ischemia on glutamate (Glu), aspartate (Asp), gamma aminobutyric acid (GABA), glutamine (Gln), glycine and taurine ) Content and the effect of adenosine triphosphate sensitive potassium channel (KATP) opener Ipac (IPK) and ketamine on the above amino acid content. Methods: The gerbil global cerebral ischemia model was prepared by ligating bilateral common carotid arteries. The contents of amino acids were determined by HPLC and fluorescence detector. Results: After bilateral carotid artery ligation for 5 min and reperfusion for 60 min, the content of Glu and Asp in hippocampus of gerbils increased by 40% and 80% respectively, and GABA, Gln, Gly and Tau also increased obviously. IPK (100 ~ -1, ip) and ketamine (120 mg · kg -1, ip) reversed ischemic-induced increases in Glu, Asp, Gln and Gly release but did not reverse ischemia-induced increases in GABA and Tau release. CONCLUSION: Neuronal injury induced by global cerebral ischemia may be related to the increase of Glu, Asp, Gln and Gly contents, while the increase of inhibitory amino acids GABA and Tau may be an important self-protection mechanism of brain. IPK reversed cerebral ischemia-induced increase of excitatory amino acids may be its biochemical basis of anti-excitotoxicity.