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大鼠一氧化碳诱导的神经病变。超微结构变化。

Carbon monoxide-induced neuropathy in the rat. Ultrastructural changes.

作者信息

Grunnet M L, Petajan J H

出版信息

Arch Neurol. 1976 Mar;33(3):158-63. doi: 10.1001/archneur.1976.00500030014003.

Abstract

The peroneal and ventral caudal nerves of rats exposed to 2,500 ppm CO until loss of nerve conduction occurred were studied by electron microscopy. Loss of normal axonal and Schwann cell structure was seen at the node of Ranvier. This loss was more prominent in large myelinated fibers, but was also seen in small myelinated fibers at seven and ten days postexposure. At this time, ventral caudal nerve conduction velocity decreased following a transient period of recovery lasting 9 to 13 days. Repair of the node began at 14 to 21 days postexposure, when maximal nerve conduction velocity had returned to normal. Complete normalization of node structure was not seen even 60 days after exposure, in many instances.

摘要

通过电子显微镜研究了暴露于2500 ppm一氧化碳直至神经传导丧失的大鼠的腓总神经和尾腹侧神经。在郎飞结处可见正常轴突和施万细胞结构的丧失。这种丧失在大的有髓纤维中更为明显,但在暴露后7天和10天的小的有髓纤维中也可见到。此时,尾腹侧神经传导速度在持续9至13天的短暂恢复后下降。暴露后14至21天开始修复郎飞结,此时最大神经传导速度已恢复正常。在许多情况下,即使在暴露后60天,郎飞结结构也未完全恢复正常。

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