A model for creating a single stretch injury in murine biarticular muscle.
A model for creating a single stretch injury in murine biarticular muscle.
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DOI：
10.1186/2052-1847-6-14
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发表时间：
2014-04-05
期刊：
影响因子：
--
通讯作者：
Vanderby R Jr
中科院分区：
文献类型：
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作者：
Brickson SL;McCabe RP;Pala AW;Vanderby R Jr
我们开发了一个单一的拉伸损伤模型，在小鼠腓肠肌的肌腱接头（MTJ）附近造成损伤。我们的假设是，肌肉损伤的程度可以通过在延长收缩之前逐步缩短跟腱（AT）来控制。缩短增加将导致损伤后24小时更大的等长扭矩不足和形态学损伤。将16只小鼠随机分配到假手术组或损伤组，损伤组的AT缩短呈阶梯状增加。暴露AT并将其放置在定制的不锈钢辊夹系统中，以实现特定的缩短水平; 0 mm（静止长度）、0.7 mm或1.4 mm。用针电极刺激跖屈肌至手足抽搐，然后以450°/秒的速度从中立位主动延长至背屈75°。被动和等距扭矩测量前和立即受伤后。损伤后24 h再次测量等距扭矩。在偏心损伤期间记录峰值等速扭矩。只有在AT缩短诱导时，损伤才导致被动和即刻绝对等长扭矩降低。AT缩短组伤后即刻和24 h的伤前等长扭矩百分比显著降低，但不受缩短水平的影响。仅在损伤后24小时，在0 mm组中观察到相对等长扭矩不足。各组受伤期间的峰值等速扭矩相似。损伤后24小时的组织学评价显示AT缩短组中MTJ附近的形态学损伤增加。单拉伸与AT缩短造成的形态学损伤附近的MTJ和等距扭矩赤字立即和24小时后损伤，但损害的程度不能滴定与AT缩短的阶梯式增加。该模型提供了一个机会，利用转基因小鼠，以阐明炎症介质，促进再生和抑制纤维化，以优化治疗干预完全功能恢复。
We developed a single stretch injury model to create damage near the musculotendinous junction (MTJ) of the gastrocnemius muscle in mice. Our hypothesis was that magnitude of muscle injury could be controlled by stepped shortening of the Achilles tendon (AT) prior to a lengthening contraction. Increased shortening would result in a greater isometric torque deficit and morphological damage 24 hours post-injury. Sixteen mice were randomly assigned to sham or injury predicated on stepped increases in AT shortening. The AT was exposed and placed in a customized stainless steel roller-clamp system to achieve a specific level of shortening; 0 mm (resting length), 0.7 mm or 1.4 mm. Plantar flexors were stimulated to tetany with a needle electrode and then actively lengthened at 450°/sec from neutral to 75° of dorsiflexion. Passive and isometric torques were measured pre- and immediately post-injury. Isometric torque was measured again 24 h post-injury. Peak isokinetic torque was recorded during eccentric injury. Injury resulted in decreased passive and immediate absolute isometric torque only when induced with AT shortening. The percentage of pre-injury isometric torque was significantly lower in the AT shortened groups immediately and 24 h post-injury, but was unaffected by the level of shortening. Relative isometric torque deficits were noted in the 0 mm group only 24 h post-injury. Peak isokinetic torque during injury was similar in all groups. Histological evaluation 24 h post-injury revealed increased morphological damage near the MTJ in the AT shortened groups. Single stretch with AT shortening created morphological damage near the MTJ and isometric torque deficits immediately and 24 h post-injury, but the magnitude of damage could not be titrated with stepped increases in AT shortening. This model provides an opportunity to utilize transgenic mice in order to elucidate inflammatory mediators that promote regeneration and inhibit fibrosis in order to optimize therapeutic interventions for complete functional recovery.