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目的研究缺氧再灌对皮层神经元的影响以及氯胺酮和右美沙芬的保护作用。方法采用１６～１８ｄ胎龄的大鼠皮层细胞分离培养，以培养上清液中乳酸脱氢酶（ＬＤＨ）活性作为细胞损伤的指标。结果培养１２ｄ的细胞先置于缺氧环境中５ｈ，再灌０～２４ｈ后，随着缺氧再灌时间延长，ＬＤＨ漏出增加。缺氧再灌前，于培养液中加入氯胺酮或右美沙芬，则ＬＤＨ漏出量均明显低于对照组。结论缺氧和再灌均造成皮层神经元严重损伤，氯胺酮和右美沙芬对上述损伤有明显的保护作用；说明ＮＭＤＡ（Ｎ－ｍｅｔｈｙｌ－Ｄ－ａｓｐａｒｔａｔｅ）受体在缺血性脑损伤过程起着至关重要的作用。
Objective To investigate the effects of anoxia-reperfusion on cortical neurons and the protective effect of ketamine and dextromethorphan. Methods Rat cortical cells from 16 to 18 days old were isolated and cultured. Lactate dehydrogenase (LDH) activity in the supernatant was used as an indicator of cell injury. Results The cells cultured for 12 days were placed in hypoxia environment for 5 hours, and after 0-24 hours of reperfusion, LDH leakage increased with the prolonged hypoxia-reperfusion time. Before hypoxia-reperfusion, LDH leakage was significantly lower than that of the control group by adding ketamine or dextromethorphan to the culture fluid. Conclusion Both hypoxia and reperfusion can cause severe damage to cortical neurons. Ketamine and dextromethorphan exert a protective effect on these injuries. This indicates that NMDA receptor plays an important role in ischemic brain injury Crucial role.