Dyck P J, O'Brien P C, Ohnishi A
J Neuropathol Exp Neurol. 1977 May;36(3):570-5.
One-hundred teased fibers of proximal and of distal sural nerve of five rats fed lead carbonate for 3 months were evaluated to see whether the pattern of segmental demyelination was random or clustered. If the evaluation was done by the length of the "territory of an old internode" (the region of one Schwann cell) a significant departure from randomness could not be shown for the majority of nerves. However, if the evaluation was by regions with and without myelin a highly clustered pattern of segmental demyelination was found. Since several remyelinated internodes form following internodal segmental demyelination, of one "old internode" the latter method of analysis would be expected to show clustering even though Schwann cell damage was random. Therefore the second method of analysis cannot be used to assess randomness of Schwann cell involvement in neuropathy. We interpret these studies as supporting the concept that Schwann cells are primarily and ubiquitously involved in lead neuropathy of the rat. Possible mechanisms of such primary Schwann cell injury are direct damage from lead of the intrafascicular interstitial fluid or from increased intrafascicular interstitial pressure.
对五只喂食碳酸铅三个月的大鼠的腓肠神经近端和远端的100根 teased 纤维进行评估,以观察节段性脱髓鞘模式是随机的还是聚集的。如果通过“旧结间段区域”(一个施万细胞的区域)的长度进行评估,大多数神经并未显示出与随机性有显著差异。然而,如果通过有髓鞘和无髓鞘区域进行评估,则发现节段性脱髓鞘呈高度聚集模式。由于节间段性脱髓鞘后会形成几个再髓鞘化的结间段,对于一个“旧结间段”,即使施万细胞损伤是随机的,后一种分析方法也会显示出聚集性。因此,第二种分析方法不能用于评估施万细胞参与神经病变的随机性。我们将这些研究解释为支持这样一种概念,即施万细胞主要且普遍地参与大鼠的铅中毒性神经病变。这种原发性施万细胞损伤的可能机制是束内间质液中的铅直接损伤或束内间质压力增加。