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缺氧、高碳酸血症和缺血时的脑能量代谢与儿茶酚胺能活性

Brain energy metabolism and catecholaminergic activity in hypoxia, hypercapnia and ischemia.

作者信息

Siesjö B K

出版信息

J Neural Transm Suppl. 1978(14):17-22.

PMID:290738
Abstract

A brief review is given of recent results which indicate that several stressful situations are accompanied by an increase in cerebral metabolic rate, mediated by extrinsic or intrinsic catecholamines. These situations include withdrawal of nitrous oxide supply in paralyzed animals ("immobilization stress"), amphetamine intoxication, hypoxia, and hypercapnia. Studies of hypercapnia (and hypoxia) suggest that activity in cerebral noradrenergic systems is enhanced by cellular acidosis. Data obtained during recirculation, following severe, transient ischemia, indicate that in spite of a general depression of cerebral metabolism (and neuronal function) some neuronal systems, notably the noradrenergic ones, show evidence of increased activity.

摘要

本文简要回顾了近期的研究结果,这些结果表明,几种应激情况会伴随着脑代谢率的增加,这是由外源性或内源性儿茶酚胺介导的。这些情况包括在瘫痪动物中停止供应一氧化二氮(“制动应激”)、苯丙胺中毒、缺氧和高碳酸血症。对高碳酸血症(和缺氧)的研究表明,细胞酸中毒会增强脑去甲肾上腺素能系统的活性。在严重短暂性缺血后的再循环过程中获得的数据表明,尽管脑代谢(和神经元功能)普遍受到抑制,但一些神经元系统,尤其是去甲肾上腺素能系统,显示出活性增加的迹象。

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Brain energy metabolism and catecholaminergic activity in hypoxia, hypercapnia and ischemia.缺氧、高碳酸血症和缺血时的脑能量代谢与儿茶酚胺能活性
J Neural Transm Suppl. 1978(14):17-22.
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