Kalliainen Loree K, Jejurikar Sameer S, Liang Lawrence W, Urbanchek Melanie G, Kuzon William M
Department of Surgery, Division of Plastic Surgery, Ohio State University, Columbus, Ohio, USA.
Muscle Nerve. 2002 Jan;25(1):31-8. doi: 10.1002/mus.1216.
Skeletal muscle demonstrates a specific force deficit after repair of injured peripheral nerves, microneurovascular muscle transfer, and normal aging. Because atrophy cannot account for deficits in specific force, other, unknown, mechanisms are responsible for the resulting muscle contractile dysfunction under these circumstances. We tested the hypothesis that a subpopulation of denervated fibers is partially or completely responsible for the specific force deficit after partial denervation of the rat extensor digitorum longus muscle (EDL). Adult Fisher rats underwent either sham exposure or partial transection of 80% of the cross-sectional area of the left deep peroneal nerve. After a 2-week recovery period, maximum isometric force (F(0)) was measured in situ and maximum specific force (sF(0)) was calculated for EDL from both control (n = 8) and partial denervation (n = 7) groups. Innervated fiber cross-sectional area (CSA(inn)) was measured directly from whole EDL cross sections after immunohistochemical labeling for neural cell adhesion molecule (NCAM), a marker of muscle fiber denervation. A corrected specific force value (sF(0-inn)) was calculated by normalizing F(0) to CSA(inn). Partial skeletal muscle denervation resulted in significant reductions in muscle mass, F(0), and sF(0). The percentage of muscle fibers expressing NCAM in the extrajunctional sarcolemma increased from 1.0 +/- 0.8% in control to 49 +/- 15% in partially denervated EDL muscles. A 62.7% deficit in EDL specific force was observed after partial denervation. Denervated muscle fibers accounted for 59.3% of this deficit, but sF(0-inn) still differed significantly between control and partially denervated muscles, with a 25.5% difference between groups. In partially denervated muscles, the specific force deficit is partially but not fully explained by a subpopulation of noncontractile, denervated fibers.
在周围神经损伤修复、显微神经血管肌肉移植以及正常衰老后，骨骼肌会出现特定的力量缺陷。由于萎缩无法解释特定力量的缺陷，在这些情况下，其他未知机制导致了肌肉收缩功能障碍。我们测试了这样一个假设：失神经支配纤维的一个亚群部分或完全导致大鼠趾长伸肌（EDL）部分去神经支配后出现特定力量缺陷。成年Fisher大鼠接受假暴露或左侧腓深神经80%横截面积的部分横断。经过2周的恢复期后，原位测量最大等长力（F(0)），并计算对照组（n = 8）和部分去神经支配组（n = 7）EDL的最大比肌力（sF(0)）。在对神经细胞黏附分子（NCAM，一种肌肉纤维失神经支配的标志物）进行免疫组织化学标记后，直接从整个EDL横切面测量有神经支配的纤维横截面积（CSA(inn)）。通过将F(0)标准化为CSA(inn)来计算校正后的比肌力值（sF(0-inn)）。部分骨骼肌去神经支配导致肌肉质量、F(0)和sF(0)显著降低。在肌膜结外表达NCAM的肌纤维百分比从对照组的1.0±0.8%增加到部分去神经支配的EDL肌肉中的49±15%。部分去神经支配后，观察到EDL比肌力有62.7%的缺陷。失神经支配的肌纤维占该缺陷的59.3%，但对照组和部分去神经支配的肌肉之间sF(0-inn)仍有显著差异，两组之间相差25.5%。在部分去神经支配的肌肉中，特定力量缺陷部分但并非完全由非收缩性失神经支配纤维亚群所解释。
