Div of Athletic Training, The Ohio State University, Columbus, OH, USA.
J Sport Rehabil. 2010 Nov;19(4):380-8. doi: 10.1123/jsr.19.4.380.
Acute musculoskeletal-injury management largely focuses on inhibiting secondary injury, although the data describing secondary injury and the timeline for its progression are sparse.
To describe the timeline and early progression of secondary injury in skeletal muscle over the first 5 h after blunt trauma.
A controlled laboratory study with 2 independent variables (injury status and postinjury time point) in a 2 × 21 factorial.
University research laboratory.
168 male Sprague Dawley rats (250 to 275 g).
Uniform blunt-contusion injury was caused to the right triceps surae using a drop-weight method; the contralateral limb served as an uninjured control. Both triceps surae were excised and flash frozen at 21 intervals across 5 h postinjury (8 animals, each 15 min).
Cytochrome-c oxidase activity via reduction of triphenyltetrazolium chloride (TTC) to triphenylformazan.
There was an interaction effect (P = .041) between and main effects for both injury status (P < .0005) and postinjury time point (P = .038). In the first 30 min after injury, uninjured tissues did not differ from injured tissues, and both displayed TTC reduction rates in the vicinity of 7.1 ± 0.94 μg × mg-1 × h-1. Statistical differences between uninjured and injured tissues became evident starting at 30 min. TTC reduction for uninjured tissues did not change, but injured tissues declined in a roughly linear fashion across the entire 5-h period to 4.8 ± 1.04 μg × mg-1 × h-1.
Cytochrome-c oxidase activity, an indicator of oxidative phosphorylation and mitochondrial viability, is diminished by events that follow muscle trauma. Loss of this enzymatic activity becomes statistically evident at 30 min postinjury and continues linearly for at least 5 h. This suggests that secondary injury is a slowly developing problem of more than 5 h duration. A window of opportunity for intervention may lie somewhere within the first 30 min after injury.
急性肌肉骨骼损伤的治疗主要集中在抑制二次损伤，尽管描述二次损伤及其进展时间的资料很少。
描述钝性创伤后 5 小时内骨骼肌中二次损伤的时间进程和早期进展。
在 2×21 因子的 2 个独立变量（损伤状态和损伤后时间点）的对照实验室研究。
大学研究实验室。
168 只雄性 Sprague Dawley 大鼠（250-275g）。
使用落体法造成右侧比目鱼肌均匀钝挫伤；对侧肢体作为未受伤的对照。在 5 小时的损伤后，通过 21 个时间间隔从每只动物的 8 只（每只动物 15 分钟）中切除并快速冷冻比目鱼肌。
通过三苯基四唑氯化物（TTC）还原为三苯基甲腙来测定细胞色素 c 氧化酶活性。
损伤状态（P<0.0005）和损伤后时间点（P=0.038）均存在交互作用（P=0.041）。在损伤后的前 30 分钟，未受伤组织与受伤组织没有差异，两者的 TTC 还原率均接近 7.1±0.94μg×mg-1×h-1。从 30 分钟开始，未受伤组织和受伤组织之间的差异变得明显。未受伤组织的 TTC 还原率没有变化，但受伤组织在整个 5 小时内呈大致线性下降，至 4.8±1.04μg×mg-1×h-1。
细胞色素 c 氧化酶活性是氧化磷酸化和线粒体活力的指标，它会受到肌肉创伤后的事件的影响。这种酶活性的丧失在损伤后 30 分钟变得明显，并持续线性至少 5 小时。这表明二次损伤是一个持续超过 5 小时的缓慢发展的问题。干预的机会可能存在于损伤后 30 分钟内。
