Katayama Y, Becker D P, Tamura T, Ikezaki K
Division of Neurosurgery, University of California, Los Angeles.
Acta Neurochir Suppl (Wien). 1990;51:271-3. doi: 10.1007/978-3-7091-9115-6_92.
Early cellular swelling following fluid-percussion brain injury was demonstrated in vivo by means of microdialysis in the rat. When rapid cellular swelling occurs, water moves from the extracellular space (ECS) into the cells and the extracellular concentration of ECS marker which does not move into the cells increases. Cellular swelling was therefore demonstrated in vivo as an increase in the dialysate concentration of 14C-sucrose ([14C-sucrose]d) pre-perfused as an ECS marker. The increase in [14C-sucrose]d occurred concomitantly with an increase in the dialysate concentration of K+ ([K+]d) representing large ionic fluxes. The increases in [K+]d and [14C-sucrose]d were both inhibited by kynurenic acid, a broad spectrum antagonist of excitatory amino acids (EAAs), which was administered through the dialysis probe. These findings suggest that early cellular swelling following traumatic brain injury is a result of ionic fluxes mediated by EAAs.
通过对大鼠进行微透析，在体内证实了流体冲击性脑损伤后早期的细胞肿胀。当快速发生细胞肿胀时，水从细胞外间隙（ECS）进入细胞，而未进入细胞的ECS标志物的细胞外浓度增加。因此，在体内，细胞肿胀表现为预先灌注作为ECS标志物的14C-蔗糖（[14C-蔗糖]d）的透析液浓度增加。[14C-蔗糖]d的增加与代表大量离子通量的K+透析液浓度（[K+]d）的增加同时发生。[K+]d和[14C-蔗糖]d的增加均受到通过透析探针给予的犬尿氨酸（一种兴奋性氨基酸（EAA）的广谱拮抗剂）的抑制。这些发现表明，创伤性脑损伤后早期的细胞肿胀是由EAA介导的离子通量的结果。
