Weller B, Karpati G, Carpenter S
Neuromuscular Research Group, Montreal Neurological Institute, P.Q., Canada.
J Neurol Sci. 1990 Dec;100(1-2):9-13. doi: 10.1016/0022-510x(90)90005-8.
Lengthening contractions were induced in the right anterior tibialis muscles (ATM) of anaesthetized normal and mdx (dystrophic) mice by supramaximal, nonfatiguing stimulation of the sciatic nerve for 180 min. In the left ATM of the same animals identical stimulation caused shortening contractions because of a prestimulation Achilles tenotomy. The prevalence of recently necrotic fibers was determined in all stimulated ATM by demonstrating the presence of IgG in the necrotic fibers using immunoperoxidase staining of cryostat sections. The results were compared to unstimulated normal and mdx ATM. A significantly higher rate of necrosis was demonstrated after lengthening contractions in the mdx ATM than normal ATM. Unstimulated normal and mdx ATM have either no or extremely infrequent necrotic fibers. We suggest that the enhanced vulnerability of mdx muscle fibers to lengthening contractions is related to the deficiency of dystrophin, which renders the sarcolemma more susceptible to suffer focal breaks. A similar situation may occur in Duchenne muscular dystrophy.
通过对坐骨神经进行超强、非疲劳性刺激180分钟，在麻醉的正常小鼠和mdx（营养不良）小鼠的右胫前肌（ATM）中诱导出延长收缩。由于预先进行了跟腱切断术，在同一动物的左ATM中相同的刺激导致缩短收缩。通过使用低温切片的免疫过氧化物酶染色显示坏死纤维中IgG的存在，确定所有受刺激的ATM中近期坏死纤维的发生率。将结果与未受刺激的正常和mdx ATM进行比较。mdx ATM在延长收缩后显示出比正常ATM显著更高的坏死率。未受刺激的正常和mdx ATM要么没有坏死纤维，要么坏死纤维极少。我们认为mdx肌纤维对延长收缩的易损性增强与肌营养不良蛋白的缺乏有关，这使得肌膜更容易遭受局灶性破裂。杜兴氏肌营养不良症可能也会出现类似情况。
