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采用１６－１８ｄ胎龄的大鼠皮层细胞分离培养，分别观察无氧再灌和谷氨酸对皮层神经元的影响以及氯胺酮的保护作用。结果如下：培养１２ｄ的细胞先置于缺氧环境中５ｈ，再灌０－２４ｈ后，随着无氧再灌时间延长，ＬＤＨ漏出增加。外源性谷氨酸也引起ＬＤＨ的漏出增加。无氧再灌和谷氨酸处理前，于培养液中加入氯胺酮，则ＬＤＨ漏出量均明显低于对照组。结果表明，无氧和再灌及过量谷氨酸均造成皮层神经元严重损伤，氯胺酮对上述损伤皆有明显的保护作用。以上结果说明谷氨酸兴奋毒性与ＮＭＤＡ受体在缺血性脑损伤过程起着至关重要的作用。
Cultured rat cortical cells aged from 16 to 18 days were used to observe the effects of anoxia and glutamate on cortical neurons and the protective effect of ketamine. The results were as follows: Cells cultured for 12 days were placed in hypoxic environment for 5h, and after 0-24h after reperfusion, LDH leakage increased with the prolongation of anaerobic reperfusion time. Exogenous glutamate also causes increased leakage of LDH. Before anaerobic reperfusion and glutamate treatment, ketamine was added to the culture medium, the LDH leakage was significantly lower than the control group. The results showed that both anoxia and reperfusion and excessive glutamate caused severe damage to cortical neurons, ketamine had obvious protective effect on the above injury. The above results suggest that glutamate excitotoxicity plays a crucial role in the process of ischemic brain injury.