Abstract
This study was designed to produce an ideal model of ischemic neuropathy, especially relevant to diabetic neuropathy (DN) with reference to vascular theory. Sprague-Dawley rats aged 11 weeks were used as experimental animals.Sodium laurate (0.3 mg) dissolved in saline (0.1 ml) was injected into the femoral artery on one side and the same volume of saline into the other side. The animals were examined clinically, electrophysiologically and histropathologically at intervals. The saline-injected leg showed no significant findings during the experimental period, whereas the laurate-injected leg manifested paresis and a persistent decrease in sciatic motor nerve conduction and low amplitudes of the muscle action potential. Histologically, swollen axons were observed with closure of microvessels on day 1 and myelin ovoids emerged on day 7. At month 1, the diameter of myelinated nerve fibers (MNFs) was significantly decreased as compared with the control side in all rats, and this was accompanied by neither increased density nor thinned myelin, suggesting fiber atrophy. Simultaneously, proliferative changes in microvessels were found and the number of nuclei in endothelial cells and the percent of closure in epineurial microvessels correlated sigfinificantly with the diameter of MNFs. At month 7, the attenuation of MNFs was more prominant and pathological changes in microvessels were persistently observed. Thus, pathological changes induced in the present study resembled some features of human DN. These results suggest that the neuropathy model induced by sodium laurate might provide a reasonably useful model for clarifying the pathogenesis of DN.
