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本文报道了用生物化学方法测定离体小鼠比目鱼肌对 HRP 的胞纳作用。结果表明,在切断神经或切腱后引起萎缩的肌肉侧或在协同肌切腱后引起代偿性肥大的肌肉侧,与它们各自对照的正常肌肉侧相比,都可发生对 HRP 胞纳的明显增加。而在肉毒杆菌毒素中毒后引起萎缩的肌肉侧,和它正常的对照肌肉侧相比,却意外地不发生这种胞纳摄取的明显增加。本文的实验结果进一步证实。肌肉的胞纳增加并不一定导致肌纤维的变性和萎缩(例如代偿性肥大的肌肉);而肌纤维的变性和萎缩亦不一定需要肌肉的胞纳增加为前提(例如肉毒杆菌毒素中毒的肌肉)。本工作结果还提示:肌肉的胞纳增加有其神经原性和肌原性因素。本文还对肌肉胞纳增加的可能机制进行了讨论。
In this paper, the biochemical effect of isolated soleus muscle on HRP in vivo was reported. The results showed that the muscle side that caused compensatory hypertrophy on the muscle side that caused atrophy after cutting nerves or tendons, or on compensatory hypertrophy after synergistic muscle tendon occurred compared to their respective control normal muscle sides obviously increase. Whereas the muscle side causing atrophy after botulinum toxin intoxication unexpectedly did not experience a significant increase in such uptake compared to its normal control muscle side. The experimental results in this paper further confirmed. Increased muscle mass does not necessarily lead to degeneration and atrophy of myofibers (eg, compensatory hypertrophy); degeneration and atrophy of myofibers also do not necessarily require an increase in myofilament (eg, botulinum toxin-poisoned muscles ). The results of this work also suggested that the increase of muscle cells have their neurogenic and myogenic factors. This article also discusses possible mechanisms for increased muscle capacity.