Kempski O S, Volk C
Institute of Neurosurgical Pathophysiology, Johannes Gutenberg-Universität Mainz, Federal Republic of Germany.
Acta Neurochir Suppl (Wien). 1994;60:7-11. doi: 10.1007/978-3-7091-9334-1_2.
During injury and ischemia of the CNS mediator compounds are released or activated which cause secondary swelling and damage of nerve cells. Such mediators are glutamate, acidosis, free fatty acids, or high extracellular potassium. Glial homeostatic mechanisms are activated to prevent the secondary injury from these mediators. The glial clearance mechanisms have been studied in detail using in vitro systems allowing for a close control of the glial environment. Current evidence suggests glial swelling to occur together with glutamate uptake or in response to extracellular acidosis. Glial swelling, therefore, is rather the result of homeostatic mechanisms than an indication of glial demise.
在中枢神经系统损伤和缺血期间，介导化合物会被释放或激活，从而导致神经细胞继发性肿胀和损伤。这些介导物包括谷氨酸、酸中毒、游离脂肪酸或细胞外高钾。神经胶质稳态机制被激活以防止这些介导物造成继发性损伤。使用能够密切控制神经胶质环境的体外系统，对神经胶质清除机制进行了详细研究。目前的证据表明，神经胶质肿胀与谷氨酸摄取同时发生或对细胞外酸中毒作出反应。因此，神经胶质肿胀更像是稳态机制的结果，而不是神经胶质死亡的迹象。
