Walz W, Klimaszewski A, Paterson I A
Department of Physiology, College of Medicine, University of Saskatchewan, Saskatoon, Canada.
Dev Neurosci. 1993;15(3-5):216-25. doi: 10.1159/000111337.
On the basis of experiments with primary cultures of mouse astrocytes with conventional K(+)-sensitive intracellular microelectrodes involving 'chemical ischemia' (antimycin a and sodium fluoride treatment), a model of ischemia is presented. According to this model, ischemia has no significant direct effect during the first 10 min on astrocytes; neurones, however, lose a major part of their K+ into the ECS. This leads to an astrocytic depolarization, which in turn activates astrocytic anion channels. This will result in passive, Donnan-mediated K+, Cl- and HCO3- fluxes into astrocytes, which in turn causes swelling and a collapse of the ECS. Arguments are put forward that this may explain the swelling of astrocytic endfeet, which occurs very early in an ischemic insult.
基于使用传统的对钾离子敏感的细胞内微电极对小鼠星形胶质细胞原代培养物进行的实验（涉及“化学性缺血”，即抗霉素A和氟化钠处理），提出了一种缺血模型。根据该模型，在最初的10分钟内，缺血对星形胶质细胞没有显著的直接影响；然而，神经元会将其大部分钾离子释放到细胞外间隙（ECS）中。这导致星形胶质细胞去极化，进而激活星形胶质细胞的阴离子通道。这将导致钾离子、氯离子和碳酸氢根离子通过被动的、唐南介导的方式流入星形胶质细胞，进而导致细胞肿胀和细胞外间隙塌陷。有人提出，这可能解释了在缺血性损伤早期就会出现的星形胶质细胞终足肿胀现象。
