Endoneurial oxygen tension and radial topography in nerve edema

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 (P_nO₂) using oxygen-sensitive microelectrodes and related P_nO₂ radial topography to ICD. We also determined local oxygen consumption (V_LO2) and critical P_nO₂ (P_critO₂). and age-matched controls were studied at 4 months. (1) Caudal nerve conduction velocity was reduced in EGN. (2) The P_nO₂ values were reduced in EGN and the P_nO₂ histogram was shifted into the hypoxic range. These changes were parallel by a significant increase in ICD in EGN. (3) The radial topography of P_nO₂ in EGN differed from the relatively uniform distribution in control nerves. In EGN the subperineurial P_nO₂ was significantly lower than the P_nO₂ at the center of the fascicle. These changes were paralleled by a significantly greater increase in ICD in the periphery. (4) That the P_nO₂ reduction in EGN was significant is suggested by the marked reduction in ·V_LO2 and the large percentage (> 75%) of intrafascicular regions that fell below P_critO₂ in EGN.