4.6 Article

Effect of aging on the biaxial mechanical behavior of human descending thoracic aorta: Experiments and constitutive modeling considering collagen crosslinking

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DOI: 10.1016/j.jmbbm.2023.105705

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Aging; Aortic stiffening; Biaxial tensile testing; Constitutive model; Crosslinking

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This study investigated the mechanical properties of the human descending thoracic aorta with aging and the role of collagen crosslinking. The results showed that the aorta stiffens with aging, especially in the longitudinal direction, leading to altered anisotropy. The constitutive modeling results suggested that excessive collagen crosslinking contributes to aortic stiffening through increased strain energy density.
Collagen crosslinking, an important contributor to the stiffness of soft tissues, was found to increase with aging in the aortic wall. Here we investigated the mechanical properties of human descending thoracic aorta with aging and the role of collagen crosslinking through a combined experimental and modeling approach. A total of 32 samples from 17 donors were collected and divided into three age groups: <40, 40-60 and > 60 years. Planar biaxial tensile tests were performed to characterize the anisotropic mechanical behavior of the aortic samples. A recently developed constitutive model incorporating collagen crosslinking into the two-fiber family model (Holzapfel and Ogden, 2020) was modified to accommodate biaxial deformation of the aorta, in which the extension and rotation kinematics of bonded fibers and crosslinks were decoupled. The mechanical testing results show that the aorta stiffens with aging with a more drastic change in the longitudinal direction, which results in altered aortic anisotropy. Our results demonstrate a good fitting capability of the constitutive model considering crosslinking for the biaxial aortic mechanics of all age groups. Furthermore, constitutive modeling results suggest an increased contribution of crosslinking and strain energy density to the biaxial stress-stretch behaviors with aging and point to excessive crosslinking as a prominent contributor to aortic stiffening.

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