Low P A, Dyck P J, Schmelzer J D
Muscle Nerve. 1982 Feb;5(2):162-5. doi: 10.1002/mus.880050214.
The effects of chronic elevations of endoneurial fluid pressure (EFP) on mammalian nerve fibers were studied using a modified model of experimental galactose neuropathy. Fiber pathology was monitored by the sensitive method of grading the pathologic abnormalities of single teased fibers. Prominent edema was produced in rats poisoned with combined oral and parenteral galactose. EFP and fascicular size were markedly elevated and tibial nerve conduction velocity was reduced. We have demonstrated, for the first time, the presence of fiber degeneration in galactose fed rats. Possible mechanisms of nerve fiber damage include: (1) impaired capillary circulation and increased fiber separation secondary to increased EFP and edema, respectively; (2) increased endoneurial hyperosmolarity, which is known to cause changes in fiber shape; and (3) unknown metabolic derangement of axons. Because much higher rates and different types of fiber pathology are encountered in lead and hexachlorophene intoxication having comparable degrees of EFP, one cannot attribute the fiber pathology directly to the raised EFP in these latter neuropathies.
使用改良的实验性半乳糖神经病模型,研究了神经内膜液压(EFP)长期升高对哺乳动物神经纤维的影响。通过对单根分离纤维的病理异常进行分级的敏感方法来监测纤维病理学变化。给大鼠经口和胃肠外联合给予半乳糖使其中毒,从而产生明显的水肿。EFP和束状大小显著升高,胫神经传导速度降低。我们首次证实在喂食半乳糖的大鼠中存在纤维变性。神经纤维损伤的可能机制包括:(1)分别由于EFP升高和水肿继发的毛细血管循环受损和纤维间距增加;(2)神经内膜高渗性增加,已知其会导致纤维形状改变;(3)轴突未知的代谢紊乱。由于在具有相当程度EFP的铅和六氯酚中毒中会出现更高发生率和不同类型的纤维病理学变化,因此不能将这些后发性神经病中的纤维病理学变化直接归因于EFP升高。