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臂丛神经损伤后不同部位肌肉萎缩的检测和机制探讨 被引量:15

Examination and mechanism of different muscles atrophy after brachial plexus injury
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摘要 目的 研究臂丛神经损伤后不同部位的失神经骨骼肌的萎缩规律 ,并探讨细胞凋亡和肌卫星细胞的变化在失神经萎缩骨骼肌中发挥的作用。 方法 臂丛神经损伤后手术治疗患者 5 0例 ,术中切取不同部位的失神经骨骼肌 80块 ,按肌肉部位分为A、B两组 ,A组为小指展肌 34块 ,B组为肱二头肌 4 6块 ,每块分别进行HE染色、Masson染色、失神经萎缩肌肉中凋亡细胞核的免疫组化染色和透射电镜观察。 结果  (1)随时间的延长 ,肌细胞萎缩愈加明显 ,A、B组在各时间段比较 ,差异均无显著性意义。(2 )失神经后骨骼肌中染成绿色的胶原纤维增多 ,早期增生并不明显 ,失神经支配 1年以上的肌肉中胶原增生更为显著。不同时间组胶原纤维与骨骼肌细胞面积比较 ,差异有显著性意义 (P <0 .0 5 ) ,同一时间段内A、B组比较 ,差异均无显著性意义。 (3)正常的骨骼肌细胞鲜见凋亡细胞核 ,失神经后骨骼肌随时间延长 ,其凋亡细胞核的数量增加 ,而小指展肌中上升速度较肱二头肌快。 (4)随着失神经时间的延长 ,肌卫星细胞含量迅速下降 ,小指展肌中肌卫星细胞下降速度较肱二头肌快。 结论 不同部位的肌肉失神经支配后 ,萎缩的肌纤维截面积及胶原纤维的增生情况相似 ,胶原纤维的增生只在晚期才成为影响神经修复手术疗效的原因之一。 Objective To observe the morphological changes of different muscles after brachial plexus injury and to investigate the role of cell apoptosis in denervation atrophy. Methods Fifty patients of brachial plexus injuries were involved. Eighty denervated muscles were harvested intraoperatively and divided into two groups: Group A (abductor digiti minimi) and Group B (biceps brachii). The slice was stained by HE staining, Masson staining and immunohistochemical staining of apoptotic nucleus. Samples were also observed under electronmicroscope for counting the satellite cells. Results There was a sharp decrease in the muscle fiber cross sectional area. There was no significant difference between Groups A and B. In both Groups A and B, a longer denervation time resulted in a more collagen fibers. The difference between Group A and Group B of same denervation time was not statistically significant. Apoptotic nucleus was rarely seen in normal skeletal muscle. With elongation of denervation time, the number of apoptotic nucleus increased. The number of abductor digiti minimi increased more rapidly than that of biceps brachii. The number of satellite cells increased slightly after denervation. Then they decreased with the elongation of denervation time, the declination of satellite cells in digiti minimi was faster than that of biceps brachii. Conclusions The changes of myofiber cross sectional area and collagen fiber content in different muscles are similar. Hyperplasia of collagen fiber only affects the treatment outcome of nerve repair in late stage. Apoptosis is closely related to muscle atrophy. Apoptosis inducing decrease of nucleus may be one of the factors influencing treatment outcome in peripheral nerve repair. And the decline of satellite cells is another reason for the poor treatment outcome.
出处 《中华创伤杂志》 CAS CSCD 北大核心 2002年第9期526-529,共4页 Chinese Journal of Trauma
基金 国家重点基础研究发展规划资助项目 (G19990 5 42 0 6)
关键词 臂丛神经损伤 肌肉萎缩 细胞凋亡 肌卫星细胞 发病机制 Brachial plexus Wounds and injuries Muscle, skeletal Muscular atrophy Apoptosis
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  • 1徐仕琦,朱盛修.运动神经断裂伤后终板改变入其临床意义[J].中华骨科杂志,1993,13(4):247-249. 被引量:12
  • 2Sunderland S. Nerve injuries and their repair: a critical apraisal. 1st ed. New York: Churchill Livingston, 1991. 241-263.
  • 3Lu DX, Huang SK, Carlson B. Electron microscopic study of long-term denervated rat skeletal muscle. Anat Rec, 1997, 248:355-365.
  • 4Borisov AB, Carlson BM. Loss of nuclei in denervated skeletal muscle:possible cellular mechanisms (abstr). FASEB J, 1995, 9:A533.
  • 5Rodrigues ADC, Schmalbruch H. Satellite cells and myonuclei in long-term denervated rat muscles. Anat Rec, 1995, 243:430-437.
  • 6田涛,吴朝晖,金惠铭,顾玉东.大鼠失神经肌萎缩后成肌细胞增殖动力学的变化[J].中华手外科杂志,1999,15(1):36-38. 被引量:16
  • 7Viguie C, Lu DX, Huang SK, et al. Quantitative study of the dffects of long-term denervation on the extensor digitorum longus muscle of the rat. Anat Rec, 1997, 248:346-354.
  • 8Carlson BM, Billington L, Faulkner JA. Studies on the regenerative recovery of long-term denervated muscle in rats. Restor Neurol Neurosci, 1996, 10:77-84.
  • 9Murray CE, Wiseman RW, Schwartz SM, et al. Skeletal myoblast transplantation for repair of muocardial necrosis. J Clin Invest, 1996, 98:2512-2523.
  • 10Irintchev A, Langer M, Zweyer M, et al. Functional improvement of damaged adult mouse muscle by implantation of primary myoblasts. J Physiol, 1997, 500(Pt3):775-785.

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