Low P A, Nukada H, Schmelzer J D, Tuck R R, Dyck P J
Brain Res. 1985 Aug 19;341(1):147-54. doi: 10.1016/0006-8993(85)91482-9.
Endoneurial edema occurs in numerous human and experimental neuropathies. We tested the hypothesis that the resultant increase in intercapillary distance (ICD) may result in endoneurial hypoxia. Experimental galactose neuropathy (EGN) was chosen since in this model, edema is due to the accumulation of galactitol, which does not directly damage nerve fibers, so that it was possible to study the role of endoneurial edema alone. We measured endoneurial oxygen tensions (PnO2) using oxygen-sensitive microelectrodes and related PnO2 radial topography to ICD. We also determined local oxygen consumption (VLO2) and critical PnO2(PcritO2). EGN and age-matched controls were studied at 4 months. (1) Caudal nerve conduction velocity was reduced in EGN. (2) The PnO2 values were reduced in EGN and the PnO2 histogram was shifted into the hypoxic range. These changes were paralleled by a significant increase in ICD in EGN. (3) The radial topography of PnO2 in EGN differed from the relatively uniform distribution in control nerves. In EGN the subperineurial PnO2 was significantly lower than the PnO2 at the center of the fascicle. These changes were paralleled by a significantly greater increase in ICD in the periphery. (4) That the PnO2 reduction in EGN was significant is suggested by the marked reduction in VLO2 and the large percentage (greater than 75%) of intrafascicular regions that fell below PcritO2 in EGN.
神经内膜水肿见于多种人类和实验性神经病变。我们检验了这样一种假说，即由此导致的毛细血管间距离（ICD）增加可能会引起神经内膜缺氧。之所以选择实验性半乳糖神经病变（EGN），是因为在这个模型中，水肿是由半乳糖醇蓄积所致，而半乳糖醇不会直接损伤神经纤维，这样就有可能单独研究神经内膜水肿的作用。我们使用氧敏感微电极测量神经内膜氧分压（PnO2），并将PnO2的径向地形图与ICD相关联。我们还测定了局部氧消耗（VLO2）和临界PnO2（PcritO2）。在4个月时对EGN组和年龄匹配的对照组进行了研究。（1）EGN组尾侧神经传导速度降低。（2）EGN组的PnO2值降低，PnO2直方图移至缺氧范围。这些变化与EGN组ICD的显著增加同时出现。（3）EGN组PnO2的径向地形图与对照神经中相对均匀的分布不同。在EGN组中，神经束膜下的PnO2显著低于神经束中心的PnO2。这些变化与外周ICD的显著更大增加同时出现。（4）EGN组VLO2的显著降低以及EGN组中超过75%的神经束内区域低于PcritO2，提示EGN组PnO2的降低是显著的。
