Objective To elucidate the underlying mechanisms of the high fatigability in mouse atrophic soleus during high-frequency tetanic contraction. 目的探讨萎缩比目鱼肌高频强直收缩疲劳性增加涉及细胞膜离子通道的可能机理。
METHODS: Isometric twitch and high-frequency tetanic contraction were examined by perfusion technique of isolated skeletal muscle strip. The contractile functions of soleus were observed in 1-week, 2-week, or 4-week tail-suspended rats. 方法:采用离体骨骼肌条灌流技术,观测模拟失重1,2和4wk大鼠比目鱼肌(SOL)等长收缩的阈刺激电压与高频强直收缩功能的动态变化。
No influence of increased frequency on fatigability of tetanic contraction in rat atrophic soleus 增加刺激频率不影响大鼠萎缩比目鱼肌强直收缩疲劳性
Conclusion These results suggest that the changes in K+ channel characteristics may increase the fatigability during high-frequency tetanic contraction in atrophic soleus. 结论萎缩比目鱼肌纤维膜上K+通道的改变,可能是引起其高频强直收缩疲劳性增加的主要因素。
During the development of the toosendanin block, the tetanic contraction of the muscle could not be maintained and the posttetanic inhibition was followed. 在川楝素作用下肌肉逐渐不能对间接强直刺激维持强直收缩,并由强直后容易化转化为强直后抑制。
P_ 33/ P_o ( P_ 33, transient tension of tetanic contraction at the 33 s) was reduced significantly in SUS, and it manifested an increase in fatigability during tetanic contraction in SUS. 但是,高频强直收缩第33秒收缩张力与最大张力之比(P33/Po)却明显降低。