CORRELATION OF THE EXTRACELLULAR GLUTAMATE CONCENTRATION WITH EXTENT OF BLOOD-FLOW REDUCTION AFTER SUBDURAL-HEMATOMA IN THE RAT

被引:132
作者
BULLOCK, R
BUTCHER, SP
CHEN, MH
KENDALL, L
MCCULLOCH, J
机构
[1] UNIV GLASGOW,INST NEUROL SCI,DEPT NEUROSURG,GLASGOW G12 8QQ,SCOTLAND
[2] UNIV GLASGOW,WELLCOME SURG INST,GLASGOW G12 8QQ,SCOTLAND
[3] UNIV EDINBURGH,DEPT PHARMACOL,EDINBURGH EH8 9YL,MIDLOTHIAN,SCOTLAND
[4] VET GEN HOSP,TAIPEI,TAIWAN
基金
英国惠康基金;
关键词
SUBDURAL HEMATOMA; GLUTAMATE; BRAIN ISCHEMIA; DIALYSIS; MICRODIALYSIS; EXCITOTOXICITY; RAT;
D O I
10.3171/jns.1991.74.5.0794
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
The excitatory neurotransmitters glutamate and aspartate are an important factor in the causation of ischemic brain damage. The concentration of glutamate and aspartate was serially measured in extracellular fluid using in vivo microdialysis after induction of a subdural hematoma or after a sham operation in the rat. Measurements were made in the cortex underlying the hematoma and in the ipsilateral hippocampus, and these findings were correlated with regional cerebral blood flow (CBF), measured autoradiographically 2 hours after hematoma induction. In the severely ischemic cortex underlying the hematoma (mean CBF < 25 ml/100 gm/min), glutamate and aspartate content increased more than 750% over basal levels. In individual animals the magnitude of glutamate release correlated with the extent of the focal ischemic zone under the hematoma (r = 0.907). Hippocampal glutamate levels rose 339%, yet regional CBF was preserved (114 ml/100 gm/min). This accords with focal hypermetabolism in this model, and may imply a glutamate-mediated "excitotoxic" process after subdural hematoma.
引用
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页码:794 / 802
页数:9
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