Journal of Okayama Medical Association
Published by Okayama Medical Association

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Full-text articles are available 3 years after publication.

曝気法における脳浮腫の実験的研究 第1編 局所脳水分量,局所脳血流量および局所神経機能の経時的変化 

門間 文行 岡山大学脳神経外科教室
100_9.pdf 4.23 MB
発行日
1988
抄録
The present experiment was designed to examine the effect of vasogenic brain edema produced by exposure to air on the electrical activity of the thalamocortical pathway and local cerebral blood flow (1CBF) measured by the hydrogen clearance method. A large area of unilateral cerebral hemisphere of anaesthetized cats was exposed to air for 12 hours, and vasogenic brain edema was produced in the cortical and subcortical structure.Water content of the primary sensorimotor cortex, white matter, and thalamus, which was measured by the specific gravity method, significantly increased by 1.9,4.1,and 0.7% g water/g tissue, respectively, after 12 hours of exposure to air. After six hours of exposure, the blood flow in the cortex, white matter, and thalamus significantly decreased from control levels of 56.8±12.7, 21.7±5,2, 44,1±13.4ml/100g/min to 46.5±13.2, 16.3±5.0, and 31.3±11.9ml/100g/min, respectively. These decreases were accompanied by diminution in the amplitude of the direct cortical responses (DCRs) and prolongation of N1 latencies of the somatosensory evoked responses (SERs) recorded at the primary sensorimotor cortex. Both electrical activities were progressively suppressed in proportion to the reduction of ICBF after six hours of exposure. These results suggest that thalamocortical ischemia is probably responsible for the neural electrical suppression observed in this experimental edema.There was a significant correlation between the amount of edema and the degree of ischemia in the white matter. Accumulation of the edema fluid may induce ischemia affecting sensory conduction through the white matter as suggested by prolongation of the N1 latency of SER.
キーワード
vasogenic brain edema
brain tissue water content
local cerebral blood flow
somatosensory evoked response
direct cortical response
ISSN
0030-1558
NCID
AN00032489