"Donor" muscle structure and function after end-to-side neurorrhaphy
"Donor" muscle structure and function after end-to-side neurorrhaphy
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DOI：
10.1097/00006534-200103000-00021
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发表时间：
2001-03-01
影响因子：
3.6
通讯作者：
Kuzon, WM
中科院分区：
文献类型：
--
作者：
Cederna, PS;Kalliainen, LK;Kuzon, WM
神经端端吻合术是神经损伤或肿瘤切除后重建周围神经的首选手术方法。然而，如果近端神经残端不能进行一期修复，则端侧神经缝合术可能是一个合理的选择。许多研究已经证明了这种技术对肌肉神经再支配的有效性。然而，很少有关于端侧神经缝合术对受“供体”神经支配的肌肉的神经支配和功能的潜在不良后遗症的信息。假设端侧神经缝合术（1）急性产生部分供体肌肉去神经支配，（2）慢性产生供体神经支配的肌肉无结构或功能缺陷。成年刘易斯大鼠被分配到两项研究中的一项，以确定端侧神经缝合对供体肌肉结构和功能的急性（2周）和慢性（6个月）影响。在急性研究中，动物接受腓神经假暴露（n = 13）或胫神经末端和腓神经侧之间的端侧神经缝合（n = 7）。2周恢复期后，测量每只动物的等长肌力（F-o），并计算趾长伸肌（“供体”肌肉）的比力（sF（o））。神经细胞粘附分子（NCAM）的免疫组织化学染色进行识别的人口失神经支配的肌纤维。在慢性研究中，动物在腓神经末端和胫神经侧面之间进行端侧神经缝合（n = 6）或假暴露胫神经并进行腓神经端端对端神经接合（n = 6），以匹配端侧神经缝合组中前室肌肉去神经支配的时间。6个月恢复期后，测量内侧腓肠肌（“供体”肌肉）的收缩特性。在端侧神经缝合的动物的供体肌肉中，失神经支配的肌纤维的百分比急剧增加了5倍（1 +/-0.7%至5.4 +/-2.7%）（p < 0.001）。然而，在这些供体肌肉中没有发现骨骼肌力缺陷。长期来看，腓肠肌内侧肌的收缩特性在假手术组和端侧神经缝合组中是相同的。这些数据支持我们的两个假设，端侧神经缝合导致急性供体肌肉失神经支配，这表明在神经接合时存在轴突的物理破坏。然而，端侧神经吻合术不影响由供体神经支配的肌肉功能的长期结构。
End-to-end nerve coaptation is the preferred surgical technique for peripheral nerve reconstruction after injury or tumor extirpation. However, if the proximal nerve stump is not available for primary repair, then end-to-side neurorrhaphy may be a reasonable alternative. Numerous studies have demonstrated the effectiveness of this technique for muscle reinnervation. However, very little information is available regarding the potential adverse sequelae of end-to-side neurorrhaphy on the innervation and function of muscles, innervated by the "donor" nerve. End-to-side neurorrhaphy is hypothesized to (1) acutely produce partial donor muscle denervation and (2) chronically produce no structural or functional deficits in muscles innervated by the donor nerve. Adult Lewis rats were allocated to one of two studies to determine the acute (2 weeks) and chronic (6 months) effects of end-to-side neurorrhaphy on donor muscle structure and function. In the acute study animals underwent either sham exposure of the peroneal nerve (n = 13) or end-to-side neurorrhaphy between the end of the tibial nerve and the side of the peroneal nerve (n = 7). After a 2-week recovery period, isometric force (F-o) was measured, and specific force (sF(o)) was calculated for the extensor digitorum longus muscle ("donor" muscle) for each animal. Immunohistochemical staining for neural cell adhesion molecule (NCAM) was performed to identify populations of denervated muscle fibers. In the chronic study, animals underwent either end-to-side neurorrhaphy between the end of the peroneal nerve and the side of the tibial nerve (n = 6) or sham exposure of the tibial nerve with performance of a peroneal nerve end-to-end nerve coaptation (n = 6), to match the period of anterior compartment muscle denervation in the end-to-side neurorrhaphy group. After a 6-month recovery period, contractile properties of the medial gastrocnemius muscle ("donor" muscle) were measured. Acutely, a fivefold increase in the percentage of denervated muscle fibers (1 +/- 0.7 percent to 5.4 +/- 2.7 percent) was identified in the donor muscles of the animals with end-to-side neurorrhaphy (p < 0.001). However, no skeletal muscle force deficits were identified in these donor muscles. Chronically, the contractile properties of the medial gastrocnemius muscles were identical in the sham and end-to-side neurorrhaphy groups. These data support our two hypotheses that end-to-side neurorrhaphy causes acute donor muscle denervation, suggesting that there is physical disruption of axons at the time of nerve coaptation. However, end-to-side neurorrhaphy does not affect the long-term structure of function of muscles innervated by the donor nerve.