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慢性氰酸钠诱发神经病变的超微结构研究

An ultrastructural study of chronic sodium cyanate-indiuced neuropathy.

作者信息

Tellez-Nagel I, Korthals J K, Vlassara H V, Cerami A

出版信息

J Neuropathol Exp Neurol. 1977 Mar-Apr;36(2):352-63.

PMID:190359
Abstract

Fifteen rats were given a sodium cyanate-rich diet for 18 months and at the end of that period, all of them had developed motor weakness and were perfused for ultrastructural study. A peripheral neuropathy involving mostly the roots and sciatic nerves was found and the main ultrastructural lesion was vacuolization of myelin. There was marked distinction of the myelin sheaths and phagocytosis of myelin. Axoplasmic changes were minimal and consisted of accumulation of glycogen within vacuoles. Invaginations of adaxonal Schwann cell membranes and axolemma forming loops and separate chambers were also present. There was active participation of macrophages in the splitting of myelin as well as in phagocytosis of myelin remnants. There was evidence of remyelination with the toxic damage. We concluded that cyanate induced neuropathy is due mostly to a myelinotoxic effect of the drug, although parallel but less intense axonal damage cannot be excluded.

摘要

15只大鼠食用富含氰酸钠的饮食18个月,在该时间段结束时,它们均出现运动无力,并进行灌注以进行超微结构研究。发现了一种主要累及神经根和坐骨神经的周围神经病变,主要的超微结构病变是髓鞘空泡化。髓鞘有明显的分层以及髓鞘的吞噬现象。轴浆变化轻微,表现为液泡内糖原积聚。轴突旁施万细胞膜和轴膜内陷形成环和独立的腔室也存在。巨噬细胞积极参与髓鞘的分裂以及髓鞘残余物的吞噬。有证据表明存在对毒性损伤的髓鞘再生。我们得出结论,氰酸盐诱导的神经病变主要是由于该药物的髓鞘毒性作用,尽管不能排除同时存在但程度较轻的轴突损伤。

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