Shibahara N, Okada S, Onishi S, Hamada K, Takasaki N, Miyazaki S, Nakagaki I, Sasaki S
Department of Urology, Osaka Medical School, Japan.
Nihon Jinzo Gakkai Shi. 1990 Aug;32(8):885-92.
We investigated the mechanism of uremic neuropathy using experimental acute and chronic renal failure models in rats. After induction of renal failure, the motor nerve conduction velocity, axoplasmic electrolyte content, and cross-sectional area of myelinated fibers in the sciatic nerve were determined. The axoplasmic Na, K, Cl, and Ca contents were measured by electron probe X-ray microanalysis employing with sections from freshly freeze-dried sciatic nerves. The results obtained for both the acute and chronic renal failure models were similar. The sciatic motor nerve conduction velocity was significantly decreased in both cases as compared to that in the controls. The sciatic nerve axoplasmic Na content was significantly lower than that of the controls in both acute and chronic renal failure, and a significant reduction in the cross-sectional area of the myelinated fibers was observed in both renal failure models. These results suggest that impairment of the axonal membrane Na permeability and shrinkage of the myelinated fibers may play an important role in the decrease of motor nerve conduction velocity in uremic neuropathy.