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实验性脑缺血:巴比妥类药物抵抗性区域葡萄糖利用增加。

Experimental cerebral ischemia: barbiturate resistant increase in regional glucose utilization.

作者信息

Nedergaard M, Diemer N H

机构信息

Department of General Physiology and Biophysics, Panum Institute, University of Copenhagen, Denmark.

出版信息

J Cereb Blood Flow Metab. 1988 Oct;8(5):763-6. doi: 10.1038/jcbfm.1988.125.

Abstract

During the first hours after experimental occlusion of the middle cerebral artery (MCA) cerebral glucose utilization increases in the tissue adjacent to ischemic focus. To test whether the increased glucose utilization was a consequence of increased neuronal activity, the effect of preocclusion pentobarbital administration was investigated. Rats in barbiturate-induced coma showed a metabolic response to MCA occlusion similar to those seen with light halothane anesthesia. This indicates that the enhanced glucose utilization adjacent to the ischemic core is not a result of increased neuronal activity.

摘要

在大脑中动脉(MCA)实验性闭塞后的最初几个小时内,缺血灶附近组织的脑葡萄糖利用率会增加。为了测试葡萄糖利用率的增加是否是神经元活动增加的结果,研究了闭塞前给予戊巴比妥的效果。处于巴比妥酸盐诱导昏迷状态的大鼠对MCA闭塞的代谢反应与轻度氟烷麻醉时相似。这表明缺血核心附近葡萄糖利用率的提高并非神经元活动增加的结果。

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