Ashmore C R, Hitchcock L, Lee Y B
Department of Animal Science, University of California, Davis 95616.
Exp Neurol. 1988 May;100(2):341-53. doi: 10.1016/0014-4886(88)90113-6.
The wings of 10 chickens between 1 and 5 years of age were passively extended. An increase in plasma creatine phosphokinase activity was observed in 30 min, continued to rise for 24 h, and then declined, suggesting mechanically induced damage to muscle fibers. Wing muscles were removed and examined histologically at various times after stretch. Patagialis muscles, but not biceps brachii, showed the development of muscle fiber pathology. The patagialis muscle is less active than the biceps brachii and is stretched to a greater degree by wing extension. Susceptibility of muscles to development of pathology appeared to be correlated with the age of the chickens. Pathology was remarkably similar to that observed in young chickens with hereditary muscular dystrophy. Necrotic fibers exhibiting segmental necrosis, abnormal shapes, enlargement, splitting, vacuolation, and phagocytosis were evident. Of particular interest was the appearance of abnormal clusters of acetylcholinesterase activity along the sarcolemma. These sites were shown to appear on fibers of 2-week-old dystrophic chicks prior to necrosis and increase in plasma creatine phosphokinase activity. It is suggested that aging of inactive muscles may promote adhesions between muscle fibers rendering them susceptible to damage when stretched and that necrosis of dystrophic fibers may be initiated by a similar mechanism. Such could occur if the genetic defect resulted in interfiber adhesions. Support for this hypothesis by other reports in the literature is discussed.
对10只1至5岁鸡的翅膀进行被动伸展。30分钟时观察到血浆肌酸磷酸激酶活性增加,持续上升24小时,然后下降,提示肌肉纤维受到机械性损伤。在伸展后的不同时间取出翅膀肌肉并进行组织学检查。翼膜肌而非肱二头肌出现了肌肉纤维病理变化。翼膜肌的活动程度低于肱二头肌,且在翅膀伸展时被拉伸的程度更大。肌肉对病理变化发展的易感性似乎与鸡的年龄有关。病理变化与患有遗传性肌肉营养不良的幼鸡所观察到的情况非常相似。可见坏死纤维呈现节段性坏死、形状异常、增大、分裂、空泡化和吞噬现象。特别有趣的是,沿肌膜出现了异常的乙酰胆碱酯酶活性簇。这些位点在2周龄营养不良雏鸡的纤维坏死和血浆肌酸磷酸激酶活性增加之前就已出现。提示不活动肌肉的老化可能会促进肌肉纤维之间的粘连,使其在伸展时易受损伤,并且营养不良纤维的坏死可能由类似机制引发。如果基因缺陷导致纤维间粘连,就可能发生这种情况。文中讨论了文献中其他报告对这一假说的支持。