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链脲佐菌素诱导的糖尿病大鼠的自主神经病变

Autonomic neuropathy in the streptozotocin diabetic rat.

作者信息

Monckton G, Pehowich E

出版信息

Can J Neurol Sci. 1980 May;7(2):135-42. doi: 10.1017/s0317167100023519.

Abstract

An ultrastructural study of the sympathetic ganglia, dorsal sympathetic chain, and Auerbach's plexus is described in the streptozotocin diabetic rat. The observations cover the first six weeks following induction of diabetes. Degenerative changes began to appear in the axonal plasma membranes and axoplasm of unmyelinated fibers at 24 hours and were widespread by two weeks. Axonal sprouting and regenerating axons began to appear and increase in number through the 6th week. Chromatolysis in ganglion cells in sympathetic ganglia became apparent by two weeks as did degenerative changes in axons of Auerbach's plexus. This somewhat later appearance of changes in ganglion cells and Auerbach's plexus suggested the primary changes occurred in the postganglionic fibers. The cycle of change from degeneration to regeneration in the areas examined suggests either a possible toxic effect of streptozotocin or a combination of metabolic disturbances as a cause of this neuropathy.

摘要

本文描述了对链脲佐菌素诱导的糖尿病大鼠交感神经节、背侧交感链和奥尔巴赫神经丛的超微结构研究。观察涵盖了糖尿病诱导后的前六周。变性变化在24小时时开始出现在无髓纤维的轴突质膜和轴浆中,并在两周时广泛存在。轴突发芽和再生轴突在第6周开始出现并数量增加。交感神经节中的神经节细胞的染色质溶解在两周时变得明显,奥尔巴赫神经丛的轴突中的变性变化也是如此。神经节细胞和奥尔巴赫神经丛中变化的这种稍晚出现表明主要变化发生在节后纤维中。在所检查区域从变性到再生的变化周期表明,链脲佐菌素可能有毒性作用,或者代谢紊乱的组合是这种神经病变的原因。

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