Pei L, Zong Y, Zhang G
Research Center of Biochemistry and Molecular Biology, Xuzhou Medical College.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 1997 May;13(2):148-50.
The effects of anoxia/reoxygenation (A/R) and glutamate on cultured cortical neurons from 16 to 18-day-old fetal rats and the protective effect of ketamine were studied. The 12-day cultures of 12 days were exposed to anoxia (5 h) followed by reoxygenation (0-24 h). Following progressive A/R, the release of lactate dehydrogenase (LDH) into the bathing medium obviously increased and exogenous glutamate (3 h) also markedly increased the release of LDH. When the cultures were pretreated with ketamine before A/R, the amounts of LDH efflux in culture medium were significantly less than those of controls. These results demonstrate that the cultured cortical neurons are seriously damaged by A/R and exogenous glutamate. Such damage could be attenuated by ketamine, suggesting that the neurotoxic effect of glutamate and NMDA (N-methyl-D-aspartate) receptors play an important role in the process of ischemia-induced damage in the brain.
研究了缺氧/复氧（A/R）和谷氨酸对16至18日龄胎鼠培养皮层神经元的影响以及氯胺酮的保护作用。将培养12天的细胞暴露于缺氧环境（5小时），随后进行复氧（0至24小时）。随着A/R程度的加重，乳酸脱氢酶（LDH）释放到培养液中的量明显增加，外源性谷氨酸（3小时）也显著增加了LDH的释放。当在A/R之前用氯胺酮预处理细胞时，培养基中LDH流出量明显少于对照组。这些结果表明，培养的皮层神经元受到A/R和外源性谷氨酸的严重损伤。氯胺酮可减轻这种损伤，提示谷氨酸和N-甲基-D-天冬氨酸（NMDA）受体的神经毒性作用在脑缺血诱导损伤过程中起重要作用。
