Subramaniam K, Kumar H, Tawhai M H
Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand.
Auckland Bioengineering Institute, University of Auckland, Auckland, New Zealand
J Appl Physiol (1985). 2017 Jul 1;123(1):79-87. doi: 10.1152/japplphysiol.00208.2016. Epub 2017 Apr 27.
As a normal part of mature aging, lung tissue undergoes microstructural changes such as alveolar air-space enlargement and redistribution of collagen and elastin away from the alveolar duct. The older lung also experiences an associated decrease in elastic recoil pressure and an increase in specific tissue elastic moduli, but how this relates mechanistically to microstructural remodeling is not well-understood. In this study, we use a structure-based mechanics analysis to elucidate the contributions of age-related air-space enlargement and redistribution of elastin and collagen to loss of lung elastic recoil pressure and increase in tissue elastic moduli. Our results show that age-related geometric changes can result in reduction of elastic recoil pressure and increase in shear and bulk moduli, which is consistent with published experimental data. All elastic moduli were sensitive to the distribution of stiffness (representing elastic fiber density) in the alveolar wall, with homogenous stiffness near the duct and through the septae resulting in a more compliant tissue. The preferential distribution of elastic proteins around the alveolar duct in the healthy young adult lung therefore provides for a more elastic tissue. We use a structure-based mechanics analysis to correlate air-space enlargement and redistribution of elastin and collagen to age-related changes in the mechanical behavior of lung parenchyma. Our study highlights that both the cause (redistribution of elastin and collagen) and the structural effect (alveolar air-space enlargement) contribute to decline in lung tissue elastic recoil with age; these results are consistent with published data and provide a new avenue for understanding the mechanics of the older lung.
作为成熟衰老过程的正常组成部分，肺组织会发生微观结构变化，如肺泡气腔扩大以及胶原蛋白和弹性蛋白从肺泡管重新分布。老年肺还会出现弹性回缩压力相关下降以及特定组织弹性模量增加的情况，但这在机制上与微观结构重塑的关系尚不清楚。在本研究中，我们使用基于结构的力学分析来阐明与年龄相关的气腔扩大以及弹性蛋白和胶原蛋白重新分布对肺弹性回缩压力丧失和组织弹性模量增加的影响。我们的结果表明，与年龄相关的几何变化会导致弹性回缩压力降低以及剪切模量和体积模量增加，这与已发表的实验数据一致。所有弹性模量对肺泡壁中刚度分布（代表弹性纤维密度）敏感，靠近导管和穿过隔膜处的均匀刚度会导致组织更柔顺。因此，健康年轻成人肺中弹性蛋白在肺泡管周围的优先分布提供了更具弹性的组织。我们使用基于结构的力学分析来关联气腔扩大以及弹性蛋白和胶原蛋白重新分布与肺实质力学行为的年龄相关变化。我们的研究强调，原因（弹性蛋白和胶原蛋白的重新分布）和结构效应（肺泡气腔扩大）都导致肺组织弹性回缩随年龄下降；这些结果与已发表的数据一致，并为理解老年肺的力学提供了新途径。
