FAILURE OF CEREBRAL BLOOD FLOW-METABOLISM COUPLING AFTER ACUTE SUBDURAL-HEMATOMA IN THE RAT

被引:38
作者
KURODA, Y
BULLOCK, R
机构
[1] UNIV GLASGOW,INST NEUROL SCI,DEPT NEUROSURG,GLASGOW G12 8QQ,SCOTLAND
[2] UNIV GLASGOW,WELLCOME SURG INST,GLASGOW G12 8QQ,SCOTLAND
基金
英国惠康基金;
关键词
ACUTE SUBDURAL HEMATOMA; BRAIN METABOLISM; CEREBRAL BLOOD FLOW; FOCAL ISCHEMIA; MIDDLE CEREBRAL ARTERY OCCLUSION;
D O I
10.1227/00006123-199212000-00012
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
WE HAVE USED a recently introduced cerebral blood flow tracer, technetium-99-DL-hexamethylpropylene amine oxime, to map regional cerebral blood flow simultaneously with measurements of glucose metabolism ([C-14]-2-deoxyglucose technique) using autoradiography. The technique was used to compare the acute effects of middle cerebral artery occlusion with the more complex events that occur after induction of an acute subdural hematoma (SDH) in the rat. Previous studies with this SDH model have shown that an infarction is induced in the cortex under the hematoma. In both models, the core of the infarct zone was associated with a reduction in both flow and metabolism to less than 15% of control values. In both models, the infarct core was surrounded by a band of tissue in which glucose metabolism increases by 60 to 70% and blood flow is reduced by the same amount. Global blood flow after the SDH was reduced by 14%, but remained unchanged after middle cerebral artery occlusion. In the hippocampus, a massive increase in metabolism (up to 157%) after SDH was accompanied by a paradoxical decrease in blood flow (32%). This discrepancy between blood flow and metabolism indicates loss of flow-metabolism coupling and provides a mechanism for infarct recruitment and delayed hippocampal damage after SDH.
引用
收藏
页码:1062 / 1071
页数:10
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