Department of Mechanical Engineering, Boston University, Boston, MA, United States.
Department of Systems Design Engineering, University of Waterloo, Waterloo, Ontario, Canada; Department of Mechanical and Manufacturing Engineering, University of Calgary, Calgary, Alberta, Canada.
J Mech Behav Biomed Mater. 2023 Dec;148:106187. doi: 10.1016/j.jmbbm.2023.106187. Epub 2023 Oct 15.
Healthy arteries are continuously subjected to diverse mechanical stimuli and adapt in order to maintain a mechanical homeostasis which is characterized by a uniform distribution of wall stresses. However, aging may compromise the homeostatic microenvironment within arteries. Structural heterogeneity has been suggested as a potential microstructural mechanism that could lead to homogeneous stress distribution across the arterial wall. Our previous study on the unfolding and stretching of the elastic lamellae revealed the underlying microstructural mechanism for equalizing the circumferential stresses through wall; inner elastic layers are wavier and unfold more than the outer layers which helps to evenly distribute lamellar stretching (Yu et al., 2018). In this study, we investigated the effect of aging on lamellar deformation and its implications for tissue homeostasis. Common carotid arteries from aged mice were imaged under a multi-photon microscope while subjected to biaxial extension and inflation at five different pressures ranging from 0 up to 120 mmHg. Lamellar unfolding during pressurization was then determined from the reconstructed cross-sectional images of elastic lamellae. Tissue-level circumferential stretch was combined with the lamellar unfolding to calculate lamellar stretching. Our results revealed that the straightness gradient of aged elastic lamellae is similar to the young ones. However, during pressurization, the inner elastic lamella of the aged mice unfolded significantly more than the inner layer in young arteries. An important finding of our study is the uneven increase in inter-lamellar space which contributed to a nonuniform stretching of the elastic lamellae of aged mice arteries, elevated stress gradient, and a shifting of the load-bearing component to adventitia. Our results shed light into the complex microstructural mechanisms that take place in aging and adversely affect arterial mechanical behavior and homeostasis.
健康的动脉不断受到各种机械刺激，并进行适应性调整，以维持机械平衡状态，其特征是壁应力均匀分布。然而，随着年龄的增长，动脉内的稳态微环境可能会受到损害。结构异质性已被认为是一种潜在的微观结构机制，可导致动脉壁的应力均匀分布。我们之前关于弹性层的展开和拉伸的研究揭示了通过壁均匀化周向应力的潜在微观结构机制；内层弹性层比外层更弯曲和展开，这有助于均匀分布层状拉伸（Yu 等人，2018 年）。在这项研究中，我们研究了衰老对层状变形的影响及其对组织平衡的意义。在多光子显微镜下对老年小鼠的颈总动脉进行成像，同时在五个不同压力（从 0 到 120mmHg）下进行双轴拉伸和膨胀。然后从弹性层的重建横截面图像中确定加压过程中层状的展开情况。将组织水平的周向拉伸与层状展开相结合，以计算层状拉伸。我们的研究结果表明，老年弹性层的直线度梯度与年轻的相似。然而，在加压过程中，老年小鼠的内层弹性层比年轻动脉的内层弹性层展开得更明显。我们研究的一个重要发现是层间空间的不均匀增加，这导致老年小鼠动脉弹性层的非均匀拉伸、应力梯度升高以及承载成分向血管外膜转移。我们的研究结果揭示了衰老过程中发生的复杂微观结构机制，这些机制对动脉的机械行为和平衡状态产生不利影响。
