Dow Douglas E, Cederna Paul S, Hassett Cheryl A, Dennis Robert G, Faulkner John A
Department of Biomedical Engineering, University of Michigan, Ann Arbor, MI 48109-2200, USA.
Restor Neurol Neurosci. 2007;25(5-6):601-10.
Prolonged denervation of skeletal muscles results in atrophy and poor recovery of motor function following delayed reinnervation. Electrical stimulation reduces denervation atrophy. We hypothesized that electrical stimulation of denervated extensor digitorum longus (EDL) muscles during a prolonged period between nerve axotomy and opportunity for reinnervation by motoneurons after nerve-repair would enhance the recovery of muscle mass, force and motor-function.
The EDL muscles of rats were denervated for 3.5 months by peroneal nerve axotomy, then repaired with an end-to-end neurorrhaphy, and allowed to recover for 6.5 months. During the period of denervation, some of the rats received a protocol of electrical stimulation that had previously been shown to dramatically attenuate the effects of denervation atrophy through 4 months. Other experimental groups included unoperated control muscles, denervated muscles, and axotomy followed immediately by nerve-repair. Final evaluations included walking track analysis, maximum force measured in situ by indirect stimulation of the nerve, and muscle mass.
The hypothesis was not supported. Electrical stimulation during the period of denervation did not enhance recovery of muscle mass, force or motor function.
The primary factors that inhibited reinnervation and recovery following delayed reinnervation were not alleviated by the electrical stimulation during the period of muscle denervation.
骨骼肌长期去神经支配会导致萎缩,且在延迟重新神经支配后运动功能恢复不佳。电刺激可减轻去神经支配性萎缩。我们假设,在神经切断术至神经修复后运动神经元重新神经支配的机会出现之间的较长时间内,对去神经支配的趾长伸肌(EDL)进行电刺激,会增强肌肉质量、力量和运动功能的恢复。
通过切断大鼠腓总神经使EDL肌肉去神经支配3.5个月,然后进行端对端神经缝合修复,并使其恢复6.5个月。在去神经支配期间,部分大鼠接受了此前已证明可在4个月内显著减轻去神经支配性萎缩影响的电刺激方案。其他实验组包括未手术的对照肌肉、去神经支配的肌肉,以及切断神经后立即进行神经修复的组。最终评估包括行走轨迹分析、通过间接刺激神经原位测量的最大力量以及肌肉质量。
该假设未得到支持。去神经支配期间的电刺激并未增强肌肉质量、力量或运动功能的恢复。
肌肉去神经支配期间的电刺激并未缓解延迟重新神经支配后抑制重新神经支配和恢复的主要因素。