Henderson A H, Cattell M R
Circ Res. 1976 Apr;38(4):289-96. doi: 10.1161/01.res.38.4.289.
The plateau phase of prolonged Sr-mediated contractions of preparations of cat and frog heart muscle was used to study the transient response to abrupt changes in load or length. An oscillatory response (total amplitude equal to or less than 5% Lmax) was obtained. Isotonic oscillations were less damped than their isometric counterparts, implying positive feedback and thus a causal role of the perturbation in length. Oscillation frequency was 2-3 HZ at 29 degrees C (Q 10, 2-3); it could be increased by epinephrine or caffeine, independently of their effects on extent of shortening; it otherwise changed as a generally constant function of the length at which the oscillation occurred, whether this was altered by changes in extracellular [Sr], frequency of contraction, or load (independent of the direction and magnitude of the preceding load step). Similar oscillatory responses were induced during Sr- or Ca-mediated contractures. Cat muscles showed an additional slower component to the oscillatory response. Transient augmentation of the velocity-length relationship after abrupt reduction in load, previously described for twitch contractions under certain conditions, appears to be analogous to the first phase of the oscillatory response studied here. Our findings indicate that the oscillation is not attributable to any mechanism intrinsic to myofilament interaction, but rather that it involves length-induced changes in the level of activation, probably mediated by Ca2+ or Sr2+. We conclude that length influences the level of activation during contraction of heart muscle.
利用猫和蛙心肌制备物中锶介导的长时间收缩的平台期,研究对负荷或长度突然变化的瞬态反应。获得了一种振荡反应(总振幅等于或小于最大长度的5%)。等张振荡的阻尼比等长振荡小,这意味着存在正反馈,因此长度扰动起到了因果作用。在29摄氏度时振荡频率为2 - 3赫兹(温度系数Q10为2 - 3);肾上腺素或咖啡因可使其增加,且与它们对缩短程度的影响无关;否则,振荡频率随振荡发生时的长度呈大致恒定的函数变化,无论这种长度变化是由细胞外[锶]的改变、收缩频率还是负荷引起的(与先前负荷阶跃的方向和大小无关)。在锶或钙介导的挛缩过程中也诱导出类似的振荡反应。猫肌肉的振荡反应还表现出一个额外的较慢成分。先前在某些条件下对单收缩所描述的负荷突然降低后速度 - 长度关系的瞬态增强,似乎与此处研究的振荡反应的第一阶段类似。我们的研究结果表明,振荡并非归因于肌丝相互作用的任何内在机制,而是涉及长度诱导的激活水平变化,可能由钙离子或锶离子介导。我们得出结论,长度会影响心肌收缩过程中的激活水平。