[TRANSFORMATION OF INDIVIDUAL CONTRACTILE RESPONSES DURING TETANUS IN FAST AND SLOW RAT SKELETAL MUSCLES].

I V Kubasov, R S Arutyunyan, E V Matrosova
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Abstract

The last contractile responses (LCRN), where N is the number of individual contractile responses within tetanus, were separated from the integral tetanic responses of fast, m. Extensor digitorum longus (m. EDL), and slow, m. Soleus, rat muscles using a computer-graphic technique. The average amplitude of LCR5 in m. Soleus at a 20 Hz stimulation rate decreased to 64 ± 9 % re the amplitude of a single contraction. As N was increasing, a restoration of LCRN was observed with their subsequent rise to values almost twofold exceeding the initial single contractile responses of that muscle (up to 211 ± 10 % for LCR50). Simultaneously, against the background of rise of individual contractile responses of these muscles, a considerable shortening of their half-life time (to ≈ 50%) and formation of a stationary plateau within LCRN were observed. In m. EDL at a 50 Hz stimulation rate only single-phase rise of LCRN was observed (up to 165 ± 18% for LCR50) without change of their half-life time and plateau formation. After the end of tetanic responses in muscles of both types a prolonged (up to 30 s) "hyper-relaxation effect was shown to develop manifested as a decrease of muscle tension with its subsequent restoration to the initial values. Possible mechanisms of these effects are discussed. It is supposed that transformation of individual contractile responses in skeletal muscles may be executed at the expense of specialized microdomains in muscle fibers regulating accumulation and extrusion levels of Ca2+ ions during tetanic activity. The possible involvement of an additional, Ca(2+)-induced Ca2+ release (CICR), in the basic, depolarization-induced Ca2+ release (DICR), is analyzed.

[破伤风时快慢大鼠骨骼肌个体收缩反应的变化]。
最后的收缩反应(LCRN),其中N是破伤风中单个收缩反应的数量,使用计算机图形技术将其与大鼠快速指长伸肌(m. EDL)和缓慢比目鱼肌(m. Soleus)的整体破伤风反应分离开来。在20 Hz刺激下,比目鱼肌LCR5的平均振幅降至单次收缩幅度的64±9%。随着N的增加,观察到LCRN的恢复,其随后的上升值几乎是该肌肉最初单次收缩反应的两倍(LCR50高达211±10%)。同时,在这些肌肉个体收缩反应上升的背景下,观察到它们的半衰期显著缩短(约50%),并在LCRN内形成一个平稳的平台。在m. EDL中,在50 Hz的刺激速率下,LCRN仅单相上升(LCR50高达165±18%),而半衰期和平台形成没有变化。在两种类型的肌肉的强直反应结束后,有很长时间(长达30秒)。“过度放松效应的发展表现为肌肉张力的降低,随后恢复到初始值。讨论了这些影响的可能机制。据推测,骨骼肌个体收缩反应的转变可能是以肌肉纤维中调节Ca2+离子在强电活动期间积累和挤压水平的专门微域为代价的。另外,Ca(2+)诱导Ca2+释放(CICR),在基本的,去极化诱导Ca2+释放(DICR)可能参与分析。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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