Giffard R G, Monyer H, Choi D W
Department of Anesthesia, Stanford University School of Medicine, CA 94305.
Brain Res. 1990 Oct 15;530(1):138-41. doi: 10.1016/0006-8993(90)90670-7.
Reduction of extracellular pH from 7.4 to 6.5 attenuated glutamate neurotoxicity in murine cortical neuronal and glial cultures, but if maintained for 24 h, resulted in morphological evidence of selective glial injury. Acid-induced gliotoxicity was examined quantitatively in cortical astrocyte cultures, using lactate dehydrogenase efflux as an index of cell damage. An exposure time of 9 h to pH 6.4 was sufficient to destroy about one third of the glia, whether or not 25 mM lactate was present. Furthermore, such acidosis increased the vulnerability of glia to injury by combined oxygen and glucose deprivation. These observations support the suggestion that the acidosis which accompanies ischemia in vivo may contribute to glial injury.
将细胞外pH从7.4降至6.5可减轻小鼠皮质神经元和神经胶质细胞培养物中的谷氨酸神经毒性,但如果维持24小时,则会导致选择性神经胶质损伤的形态学证据。使用乳酸脱氢酶外排作为细胞损伤指标,在皮质星形胶质细胞培养物中对酸诱导的神经胶质毒性进行了定量检测。无论是否存在25 mM乳酸,暴露于pH 6.4 9小时就足以破坏约三分之一的神经胶质细胞。此外,这种酸中毒增加了神经胶质细胞对联合缺氧和葡萄糖剥夺损伤的易感性。这些观察结果支持以下观点,即体内缺血伴随的酸中毒可能导致神经胶质损伤。