Swanson R A, Chen J, Graham S H
Department of Neurology, Veterans Affairs Medical Center, San Francisco, California 94121.
J Cereb Blood Flow Metab. 1994 Jan;14(1):1-6. doi: 10.1038/jcbfm.1994.1.
Astrocytes in culture can maintain glutamate uptake during hypoxia if glucose is available. To determine whether this capacity is shared by brain in situ, extracellular glutamate levels were measured in ischemic brain under conditions of continued glucose delivery. Microdialysis probes were placed bilaterally in caudate nuclei of rats and perfused with artificial cerebrospinal fluid (CSF) containing either 30 or 0 mM glucose. Global cerebral ischemia was induced by cardiac arrest. Dialysate collected from probes not perfused with glucose showed a 50-fold increase in glutamate levels over the 60 min following cardiac arrest. Addition of glucose to the perfusate reduced the glutamate rise to < 20% of the levels attained in the glucose-free probes. The glucose effect was negated by the addition of 0.5 mM of the glutamate uptake blocker threo-beta-hydroxyaspartate to the artificial CSF. These results show that oxygen is not required to maintain efficient uptake of extracellular glutamate in brain and suggest that elevations in extracellular glutamate levels during ischemia result from metabolic perturbations other than hypoxia.
培养中的星形胶质细胞在缺氧且有葡萄糖供应时能够维持谷氨酸摄取。为了确定脑原位是否也具备这种能力，在持续提供葡萄糖的条件下，对缺血脑中的细胞外谷氨酸水平进行了测量。将微透析探针双侧植入大鼠尾状核，并灌注含30 mM或0 mM葡萄糖的人工脑脊液（CSF）。通过心脏骤停诱导全脑缺血。未灌注葡萄糖的探针收集的透析液显示，心脏骤停后60分钟内谷氨酸水平增加了50倍。向灌注液中添加葡萄糖可将谷氨酸的升高幅度降低至无葡萄糖探针所达到水平的<20%。向人工脑脊液中添加0.5 mM谷氨酸摄取阻滞剂苏-β-羟基天冬氨酸可消除葡萄糖的作用。这些结果表明，维持脑内细胞外谷氨酸的有效摄取并不需要氧气，并提示缺血期间细胞外谷氨酸水平的升高是由缺氧以外的代谢紊乱引起的。
