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肌肉挫伤损伤模型。生物力学、生理学和组织学。

A muscle contusion injury model. Biomechanics, physiology, and histology.

作者信息

Crisco J J, Jokl P, Heinen G T, Connell M D, Panjabi M M

机构信息

Department of Orthopaedics and Rehabilitation, Yale University School of Medicine, New Haven, Connecticut 06520-8071.

出版信息

Am J Sports Med. 1994 Sep-Oct;22(5):702-10. doi: 10.1177/036354659402200521.

DOI:10.1177/036354659402200521
PMID:7810797
Abstract

We developed a reproducible muscle contusion injury and studied its effect on contractile function, histology, and passive failure. An instrumented drop-mass technique (mass, 171 g; height, 102 cm; spherical radius, 6.4 mm) delivered a single impact to the posterior surface of the gastrocnemius muscle in one limb of 40 male Wistar rats. On Day 0, the impact significantly (N = 12, P < 0.01) decreased maximum tetanic tension to 63% of the contralateral control value. Histologic examination demonstrated extravasation of erythrocytes, edema, myofiber disruption, and vacuolation of myofibers. Passive failure initiated at the site of injury. At 2 days, tetanic tension was 75% of controls (N = 11, P < 0.01). Histologically, acute inflammation and phagocytosis were noted. Tetanic tension at 7 days was 81% of controls (N = 8, P < 0.01). Vimentin staining indicated a dramatic increase in myoblast activity. Contractile strength was near normal at 24 days. Histologic examination showed complete regeneration of normal striated muscle fibers. No vimentin activity was found. No passive failures initiated at the injury site. Contusion injury produced a significant deficit in contractile function that continually diminished with gross histologic evidence of degeneration, regeneration, and normalization at the injured muscle fibers.

摘要

我们建立了一种可重复的肌肉挫伤损伤模型,并研究了其对收缩功能、组织学和被动衰竭的影响。采用一种仪器化的落锤技术(质量171克;高度102厘米;球形半径6.4毫米),对40只雄性Wistar大鼠一侧肢体的腓肠肌后表面施加单次撞击。在第0天,撞击显著(N = 12,P < 0.01)降低了最大强直张力,降至对侧对照值的63%。组织学检查显示有红细胞外渗、水肿、肌纤维断裂和肌纤维空泡化。被动衰竭始于损伤部位。在第2天,强直张力为对照值的75%(N = 11,P < 0.01)。组织学上,可见急性炎症和吞噬作用。在第7天,强直张力为对照值的81%(N = 8,P < 0.01)。波形蛋白染色表明成肌细胞活性显著增加。在第24天时收缩强度接近正常。组织学检查显示正常横纹肌纤维完全再生。未发现波形蛋白活性。损伤部位未出现被动衰竭。挫伤损伤导致收缩功能显著缺陷,随着损伤肌纤维出现变性、再生和正常化的大体组织学证据,这种缺陷持续减轻。

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