Childers Martin K, Okamura Carol S, Bogan Daniel J, Bogan Janet R, Petroski Gregory F, McDonald Kerry, Kornegay Joe N
Departments of Physical Medicine and Rehabilitation, College of Veterinary Medicine, University of Missouri-Columbia, One Hospital Drive, Columbia, MO 65212, USA.
Arch Phys Med Rehabil. 2002 Nov;83(11):1572-8. doi: 10.1053/apmr.2002.35109.
To test the hypothesis that eccentric contractions induce greater injury in dystrophic compared with normal canine muscle.
Blinded cohort study.
Animal laboratory.
Ten dogs with a homologue to Duchenne muscular dystrophy (Golden retriever muscular dystrophy [GRMD]) and 10 normal littermates.
Contractions induced in tibiotarsal flexors and extensors by sciatic nerve stimulation. Because more powerful extensors overrode flexors, eccentric contractions occurred in flexors. Concentric contractions were induced in contralateral flexors by peroneal nerve stimulation.
Tibiotarsal flexion force 3 days after contractions. Muscle was examined for injury (esterase activity, Evans blue dye penetration) and regeneration (embryonic myosin isoform expression).
Mean force deficit after eccentric flexor contractions was 43.3%+/-25.7% in GRMD dogs compared with 25.0%+/-18.4% in controls (P=.04, Wilcoxon rank-sum test). Concentric contractions induced force deficits in GRMD but not normal dogs; however, the difference between the 2 groups was not significant (P=.08, Wilcoxon rank-sum test). After concentric contractions in controls, force decrements correlated with esterase activity measured by area (r=.794, P=.006) and intensity (r=.697, P=.025, Spearman rank correlation). No other significant correlation was detected between force and biopsy data.
Force data support the hypothesis that eccentric contractions induce greater injury in dystrophic compared with normal canine muscle. Phenotypic features of the dystrophic canine model used here are similar to those of humans with Duchenne's.
验证与正常犬类肌肉相比,离心收缩在营养不良性肌肉中会导致更严重损伤这一假设。
盲法队列研究。
动物实验室。
10只患有与杜氏肌营养不良症同源疾病(金毛寻回犬型肌营养不良症[GRMD])的犬以及10只正常同窝出生的犬。
通过坐骨神经刺激诱导胫跗关节屈肌和伸肌收缩。由于伸肌力量更强而超过屈肌,因此屈肌发生离心收缩。通过腓总神经刺激在对侧屈肌中诱导向心收缩。
收缩后3天的胫跗关节屈曲力。检查肌肉的损伤情况(酯酶活性、伊文思蓝染料渗透情况)和再生情况(胚胎型肌球蛋白同工型表达)。
GRMD犬离心性屈肌收缩后的平均力量缺失为43.3%±25.7%,而对照组为25.0%±18.4%(P = 0.04,Wilcoxon秩和检验)。向心收缩在GRMD犬中导致力量缺失,但在正常犬中未导致力量缺失;然而,两组之间的差异不显著(P = 0.08,Wilcoxon秩和检验)。在对照组进行向心收缩后,力量下降与通过面积测量的酯酶活性(r = 0.794,P = 0.006)和强度(r = 0.697,P = 0.025,Spearman等级相关性)相关。在力量与活检数据之间未检测到其他显著相关性。
力量数据支持以下假设,即与正常犬类肌肉相比,离心收缩在营养不良性肌肉中会导致更严重损伤。此处使用的营养不良性犬模型的表型特征与杜氏肌营养不良症患者的相似。