Transient oscillatory force-length behavior of activated airway smooth muscle
Transient oscillatory force-length behavior of activated airway smooth muscle
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DOI：
10.1152/ajplung.00095.2009
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发表时间：
2009-08-01
影响因子：
4.9
通讯作者：
Lauzon, A. -M.
中科院分区：
文献类型：
--
作者：
Bates, J. H. T.;Bullimore, S. R.;Lauzon, A. -M.
Bates JH，Bullimore SR，Politi AZ，Sneyd J，Ancarte RC，Lauzon AM.激活气道平滑肌的瞬时振荡力-长度行为。Am J Physiol Lung Cell Mol Physiol 297：L362-L372，2009。首次发表于2009年6月12日; doi：10.1152/ajplung.00095.2009。气道平滑肌（ASM）在呼吸过程中周期性伸展，即使在活动状态下，但决定其动态力-长度行为的因素仍不完全清楚。我们开发了一个模型的激活ASM条，并比较其行为中观察到的大鼠气管肌条乙酰甲胆碱刺激。该模型由一个非线性粘弹性元件（开尔文体）串联的力发生器服从希尔力-速度关系。模型中的等轴力正比于约束横桥的数量，其附着遵循一级动力学。横桥的分离速度与肌肉长度的变化速度成正比。该模型准确地占实验观察到的瞬态和稳态振荡力长度行为的被动和激活ASM。然而，该模型不能预测激活的ASM条短暂地进行大的拉伸时看到的等长力的持续递减。我们推测，这种力的递减反映了一些机制无关的循环的横桥，这可能是参与逆转支气管收缩诱导的肺在体内的深充气。
Bates JH, Bullimore SR, Politi AZ, Sneyd J, Anafi RC, Lauzon AM. Transient oscillatory force-length behavior of activated airway smooth muscle. Am J Physiol Lung Cell Mol Physiol 297: L362-L372, 2009. First published June 12, 2009; doi:10.1152/ajplung.00095.2009.-Airway smooth muscle (ASM) is cyclically stretched during breathing, even in the active state, yet the factors determining its dynamic force-length behavior remain incompletely understood. We developed a model of the activated ASM strip and compared its behavior to that observed in strips of rat trachealis muscle stimulated with methacholine. The model consists of a non-linear viscoelastic element ( Kelvin body) in series with a force generator obeying the Hill force-velocity relationship. Isometric force in the model is proportional to the number of bound crossbridges, the attachment of which follows first-order kinetics. Crossbridges detach at a rate proportional to the rate of change of muscle length. The model accurately accounts for the experimentally observed transient and steady-state oscillatory force-length behavior of both passive and activated ASM. However, the model does not predict the sustained decrement in isometric force seen when activated strips of ASM are subjected briefly to large stretches. We speculate that this force decrement reflects some mechanism unrelated to the cycling of crossbridges, and which may be involved in the reversal of bronchoconstriction induced by a deep inflation of the lungs in vivo.