大鼠皮神经卡压模型的实验研究

Model study of cutaneous nerve entrapment in the rat

目的:建立大鼠皮神经卡压模型,并探讨皮神经卡压损伤的病理生理改变。方法:借鉴Mackinnon设计的周围神经卡压模型所采用的方法,分别用不同内径的硅胶管套在大鼠的隐神经上,以产生不同程度的皮神经卡压。将40只大鼠随机分成5组,每组8只。A组:隐神经不做任何处理;B组:只将隐神经适当游离,不进行卡压处理;C、D、E组:分别用内径为0.3、0.4、0.5mm的硅胶管卡压隐神经。卡压1周后,各组分别进行大体形态观察、电生理学检测和组织学检测。结果:电生理学检测显示B、E、D组的神经传导速度较A组依次减慢,C组则未引出动作电位。组织学检测:B组的神经无明显异常改变。各卡压组神经均发生不同程度的脱髓鞘改变,其中E组改变最轻,C组改变最显著,并伴有明显的瓦勒氏变性。结论:①大鼠隐神经卡压模型是一个较为理想的皮神经急性或亚急性卡压动物模型;②皮神经急性或亚急性卡压的病理生理改变过程为首先髓鞘受累发生髓鞘变形、脱髓鞘改变,使神经传导速度减慢。继而轴索受累出现轴突碎裂、溃变,神经纤维发生瓦勒氏变性,导致神经传导阻滞。

Objective：To develop a model of cutaneous nerve entrapment in the rat and investigate the pathophysiological changes of entrapment injury. Methods：With the Silastic tube banding technique designed by Mackinnon, Silastic tubes of varied internal diameters were used to band the saphenous nerves of rats to produce graded nerve entrapment injury. Forty Wistar rats were randomly divided into 5 groups（ with 8 rats in each group）. No operation was performed in group A;the saphenous nerves were freed without nerve entrapment in group B ;the saphenous nerves were banded with a Silastic tube of internal diameter 0. 3,0. 4,0. 5 mm in group C, D and E respectively. Gross morphological evaluations, electrophysiological and histological examination were done 1 week after banding. Results：The electrophysiological examination showed that the nerve conduction velocity of group B ,E, D decreased progressively compared to that of group A. No electrical conduction could be obtained in group C. No histological changes were noted in group B. Demyelination was present in all banded groups at different extent, the mildest in group E and the most distinct in group C. Besides, group C showed Wallerian degeneration. Conclusion：①The model of saphenous nerve entrapment in the rat is a fairly ideal acute or subacute animal model of cutaneous nerve entrapment. ②In the animal model of acute or subacute nerve entrapment the early pathophysiological changes are deformation of myelin sheath and demyelination which results in progressive decrease of nerve conduction velocity, then followed by axonal break and Wallerian degeneration of never fiber which results in the complete nerve conduction block.