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半乳糖中毒大鼠的周围神经传导研究。证明由于糖醇积累导致神经内膜水肿,对缺血性传导的抵抗力增加。

Peripheral nerve conduction studies in galactose-poisoned rats. Demonstration of increased resistance to ischemic conduction associated with endoneurial edema due to sugar alcohol accumulation.

作者信息

Low P A, Schmelzer J D

出版信息

J Neurol Sci. 1983 Jun;59(3):415-21. doi: 10.1016/0022-510x(83)90026-6.

Abstract

Edematous nerves of galactose-poisoned rats had an increased resistance to ischemic conduction block when compared with control animals. Ischemia was caused by cardiac arrest due to intracardiac air embolism in 1 group and by occlusion of the abdominal aorta in another. In these 2 groups of galactose-fed rats, time to 50% conduction block was increased by 27 and 42%, respectively and the difference between control and galactose rats was significant (P less than 0.01 and P less than 0.001).

摘要

与对照动物相比,半乳糖中毒大鼠的水肿神经对缺血性传导阻滞的耐受性增强。一组通过心内空气栓塞导致心脏骤停引起缺血,另一组通过阻断腹主动脉引起缺血。在这两组喂食半乳糖的大鼠中,分别有50%的传导阻滞时间增加了27%和42%,对照大鼠和半乳糖大鼠之间的差异具有显著性(P小于0.01和P小于0.001)。

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