Ludwig M S, Robatto F M, Simard S, Stamenović D, Fredberg J J
Meakins-Christie Laboratories, Royal Victoria Hospital, McGill University, Montreal, Quebec, Canada.
J Appl Physiol (1985). 1992 Apr;72(4):1332-7. doi: 10.1152/jappl.1992.72.4.1332.
Research in the mechanics of soft tissue, and lung tissue in particular, has emphasized that dissipative processes depend predominantly on the viscous stress. A corollary is that dissipative losses may be expressed as a tissue viscous resistance, (Rti). An alternative approach is offered by the structural damping hypothesis, which holds that dissipative processes within soft tissue depend directly more on the elastic stress than on the viscous stress. This implies that dissipative and elastic processes within lung tissues are coupled at a fundamental level. We induced alterations of Rti by exposing canines to aerosols of the constrictors prostaglandin F2 alpha, histamine, and methacholine and by changing volume history. Using the structural damping paradigm, we could separate those alterations in Rti into the product of two distinct contributions: change in the coefficient of coupling of dissipation to elastance (eta) and change in the elastance itself (Edyn). Response of Edyn accounted for most of the response of resistance associated with contractile stimulation; it accounted for almost all the response associated with differences in volume history. The eta changed appreciably with constriction but accounted for little of the response of Rti with volume history. According to the structural damping hypothesis, induced changes in eta with constriction must reflect changes in the kinetics of the stress-bearing process, i.e., differences in cross-bridge kinetics within the target contractile cell and/or differences in the influence of the target cell on other stress-bearing systems. We conclude that, regardless of underlying processes, the structural damping analysis demonstrates a fundamental phenomenological simplification: when Edyn responds, Rti is obligated to respond to a similar degree.
对软组织力学，尤其是肺组织力学的研究强调，耗散过程主要取决于粘性应力。一个必然结果是，耗散损失可以表示为组织粘性阻力（Rti）。结构阻尼假说提供了另一种方法，该假说认为软组织内的耗散过程更直接地取决于弹性应力而非粘性应力。这意味着肺组织内的耗散和弹性过程在基本层面上是耦合的。我们通过让犬暴露于收缩剂前列腺素F2α、组胺和乙酰甲胆碱的气溶胶中以及改变容积历程来诱导Rti的改变。使用结构阻尼范式，我们可以将Rti的那些改变分离为两个不同贡献的乘积：耗散与弹性耦合系数（η）的变化和弹性本身（Edyn）的变化。Edyn的反应占与收缩刺激相关的阻力反应的大部分；它几乎占了与容积历程差异相关的所有反应。η随收缩有明显变化，但在Rti随容积历程变化的反应中占比很小。根据结构阻尼假说，收缩时诱导的η变化必定反映了承受应力过程动力学的变化，即目标收缩细胞内横桥动力学的差异和/或目标细胞对其他承受应力系统影响的差异。我们得出结论，无论潜在过程如何，结构阻尼分析都表明了一种基本的现象学简化：当Edyn发生反应时，Rti必然会有类似程度的反应。
