Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.
Biophys J. 2010 Nov 17;99(10):3164-71. doi: 10.1016/j.bpj.2010.09.031.
Although the active properties of airway smooth muscle (ASM) have garnered much modeling attention, the passive mechanical properties are not as well studied. In particular, there are important dynamic effects observed in passive ASM, particularly strain-induced fluidization, which have been observed both experimentally and in models; however, to date these models have left an incomplete picture of the biophysical, mechanistic basis for these behaviors. The well-known Huxley cross-bridge model has for many years successfully described many of the active behaviors of smooth muscle using sliding filament theory; here, we propose to extend this theory to passive biological soft tissue, particularly ASM, using as a basis the attachment and detachment of cross-linker proteins at a continuum of cross-linker binding sites. The resulting mathematical model exhibits strain-induced fluidization, as well as several types of force recovery, at the same time suggesting a new mechanistic basis for the behavior. The model is validated by comparison to new data from experimental preparations of rat tracheal airway smooth muscle. Furthermore, experiments in noncontractile tissue show qualitatively similar behavior, suggesting support for the protein-filament theory as a biomechanical basis for the behavior.
尽管气道平滑肌(ASM)的主动特性已经引起了广泛的建模关注,但被动机械特性的研究还不够充分。特别是,在被动 ASM 中观察到了重要的动态效应,特别是应变诱导的流体化,这在实验和模型中都得到了观察;然而,迄今为止,这些模型对于这些行为的生物物理、机械基础的描述并不完整。著名的赫胥黎交联桥模型多年来一直使用滑动丝理论成功地描述了平滑肌的许多主动行为;在这里,我们提议使用交联蛋白在交联结合位点连续体上的附着和脱附作为基础,将该理论扩展到被动生物软组织,特别是 ASM。由此产生的数学模型表现出应变诱导的流体化,以及几种类型的力恢复,同时为这种行为提供了一种新的机械基础。该模型通过与大鼠气管气道平滑肌的新实验结果进行比较得到了验证。此外,非收缩组织中的实验表现出定性上相似的行为,这表明蛋白丝理论作为该行为的生物力学基础得到了支持。