Maxwell I C, Le Quesne P M
J Neurol Sci. 1979 Sep;43(1):95-110. doi: 10.1016/0022-510x(79)90075-3.
After 2-3 weeks exposure to hexachlorophane, maximum motor nerve conduction velocity in sciatic nerves of rats was reduced by 7.5% and evoked muscle action potential amplitude by 9%. Histological examination at this stage showed intramyelin oedema affecting some fibres and axonal degeneration of other fibres. After longer periods of exposure velocity and amplitude fell further. Velocity was reduced by 27% after 6-7 months treatment. In addition to intramyelin oedema and axonal degeneration, segmental demyelination was present in animals intoxicated for more than three months. There was no correlation between the degree of oedema and reduction of conduction velocity. It is concluded that intramyelin oedema has little or no effect on conduction velocity. Nodes of Ranvier are normal in the early stages of the lesion and this may contribute to the preservation of normal conduction. The electrophysiological findings can be attributed to secondary changes of axonal degeneration and segmental demyelination.
在大鼠坐骨神经暴露于六氯酚2 - 3周后,其最大运动神经传导速度降低了7.5%,诱发肌肉动作电位幅度降低了9%。此阶段的组织学检查显示,髓鞘内水肿影响了一些纤维,其他纤维则发生轴突变性。暴露时间更长后,速度和幅度进一步下降。治疗6 - 7个月后,速度降低了27%。除了髓鞘内水肿和轴突变性外,中毒超过三个月的动物还出现节段性脱髓鞘。水肿程度与传导速度降低之间没有相关性。得出的结论是,髓鞘内水肿对传导速度几乎没有影响。在病变早期,郎飞结是正常的,这可能有助于维持正常传导。电生理结果可归因于轴突变性和节段性脱髓鞘的继发性变化。