Department of Otolaryngology, Vanderbilt University, Nashville, Tennessee, U.S.A.
Laryngoscope. 2014 May;124(5):E180-7. doi: 10.1002/lary.24454. Epub 2013 Nov 19.
OBJECTIVES/HYPOTHESIS: Previously, electrical stimulation of denervated canine laryngeal muscle was shown to promote reinnervation by native over foreign motoneurons. The goal of this study was to assess the effect of different stimulus paradigms on reinnervation quality and functional recovery.
A prospective study of six canines over 8 to 20 months.
A clinical model of laryngeal paralysis was used, where recurrent laryngeal nerves of the animals were sectioned and ventilation compromised. The abductor, posterior cricoarytenoid (PCA) muscles were implanted bilaterally with electrodes from an implantable pulse generator. Animals were randomly assigned to three groups to assess the effect of different stimulus paradigms: 1) 40 pulses per second (pps) train, 2) 10 pps train, 3) no stimulation. Spontaneous vocal fold movement was measured endoscopically during hypercapnia. Exercise tolerance was measured on a treadmill using pulse oximetry. In the terminal session, electromyography (EMG) potentials were recorded during superior laryngeal nerve stimulation to index foreign reinnervation of the PCA by reflex glottic closure (RGC) motoneurons.
After reinnervation started, nonstimulated and stimulated 40 pps animals displayed paradoxical closure of the glottis during hypercapnia and severely decreased exercise tolerance due to faulty reinnervation. In contrast, stimulated 10 pps animals displayed minimal paradoxical closure and normal exercise tolerance (12 minutes up to 8 mph). EMG findings in this group demonstrated significantly less PCA reinnervation by foreign RGC motoneurons.
PCA stimulation with low frequency reduced synkinetic reinnervation by foreign RGC motoneurons. Paradoxical closure of the glottis with inspiration was reduced and exercise tolerance restored to normal.
目的/假设：先前的研究表明，去神经犬喉肌的电刺激可促进内源性运动神经元对其的再支配，而外源性运动神经元则不能。本研究旨在评估不同刺激模式对再支配质量和功能恢复的影响。
一项为期 8 至 20 个月的六只犬前瞻性研究。
采用犬喉麻痹的临床模型，切断动物的喉返神经并导致通气受损。将可植入脉冲发生器的双侧电极植入外展肌和后环杓肌。动物被随机分配到三组，以评估不同刺激模式的影响：1）40 脉冲/秒（pps）的刺激，2）10 pps 的刺激，3）无刺激。在高碳酸血症期间通过内窥镜测量声带的自发运动。使用脉搏血氧饱和度仪在跑步机上测量运动耐量。在最后一次实验中，通过记录喉上神经刺激时的肌电图（EMG）电位，评估 PCA 由反射性声门关闭（RGC）运动神经元引起的外源性再支配。
再支配开始后，未受刺激和接受 40 pps 刺激的动物在高碳酸血症期间显示出声门的反常关闭，并且由于错误的再支配，运动耐量严重降低。相比之下，接受 10 pps 刺激的动物显示出最小的反常关闭和正常的运动耐量（高达 8 英里/小时，12 分钟）。该组的 EMG 结果表明，PCA 由外源性 RGC 运动神经元的再支配显著减少。
低频刺激 PCA 可减少外源性 RGC 运动神经元的同步性再支配。吸气时的声门反常关闭减少，运动耐量恢复正常。
