Hovda D A, Yoshino A, Kawamata T, Katayama Y, Fineman I, Becker D P
Division of Neurosurgery, UCLA School of Medicine.
Acta Neurochir Suppl (Wien). 1990;51:331-3. doi: 10.1007/978-3-7091-9115-6_112.
Immediately following a lateral fluid percussion brain injury, the cerebral cortex and hippocampus ipsilateral to the percussion show a marked accumulation of calcium and a pronounced increase in glucose metabolism. To determine if this increase in glucose metabolism was related to the indiscriminate release of the excitatory amino acid (EAA) glutamate, kynurenic acid (an EAA antagonist) was perfused into the cerebral cortex through a microdialysis probe for 30 min prior to injury. The results show that adding kynurenic acid to the extracellular space prior to trauma prevents the injury-induced increase in glucose utilization. These results indicate that calcium contributes to the ionic fluxes that are typically seen following brain injury and supports the concept of an increased energy demand upon cells to drive pumping mechanisms in order to restore membrane ionic balance.
在侧方流体冲击性脑损伤后，冲击同侧的大脑皮层和海马体立即出现钙的显著积聚以及葡萄糖代谢的明显增加。为了确定这种葡萄糖代谢的增加是否与兴奋性氨基酸（EAA）谷氨酸的无差别释放有关，在损伤前30分钟通过微透析探针将犬尿氨酸（一种EAA拮抗剂）灌注到大脑皮层中。结果表明，在创伤前将犬尿氨酸添加到细胞外空间可防止损伤诱导的葡萄糖利用增加。这些结果表明，钙促成了脑损伤后通常出现的离子通量，并支持了细胞能量需求增加以驱动泵机制来恢复膜离子平衡这一概念。
