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大鼠链脲佐菌素糖尿病中的巨大轴索性神经病

Giant axonopathy in streptozotocin diabetes of rats.

作者信息

Jirmanová I

机构信息

Institute of Physiology, Academy of Sciences, Czech Republic, Prague.

出版信息

Acta Neuropathol. 1993;86(1):42-8. doi: 10.1007/BF00454897.

Abstract

The ultrastructure of peripheral sensory nerves was investigated in adult Wistar rats suffering from experimental diabetes mellitus 6 and 10 weeks after the injection of streptozotocin. Giant axons were seen in sections from the nerves of streptozotocin-treated rats; some contained masses of neurofilaments, others were predominantly filled with ill-defined vesicles. At the swollen axons, the myelin sheath was thinned or absent. In other regions, large intramyelinic vacuoles were observed. A number of nerve fibers broke down completely and underwent Wallerian degeneration. This was accompanied by Schwann cell proliferation and formation of Büngner bands. Concomitantly with axonal degeneration, nerve regeneration started from intact internodes. The pathomorphology of streptozotocin diabetic neuropathy closely resembles that of some toxic distal axonopathies. This points to a common metabolic basis of giant axonopathies of different etiology.

摘要

在注射链脲佐菌素6周和10周后患有实验性糖尿病的成年Wistar大鼠中,研究了外周感觉神经的超微结构。在链脲佐菌素治疗大鼠的神经切片中可见巨大轴突;一些含有大量神经丝,另一些主要充满不明确的小泡。在肿胀的轴突处,髓鞘变薄或缺失。在其他区域,观察到大量髓鞘内空泡。许多神经纤维完全分解并发生华勒变性。这伴随着施万细胞增殖和形成许旺氏带。与轴突变性同时,神经再生从完整的节间开始。链脲佐菌素糖尿病性神经病变的病理形态学与某些毒性远端轴索性神经病非常相似。这表明不同病因的巨大轴索性神经病有共同的代谢基础。

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