Brunel Institute for Bioengineering, Brunel University London, Kingston Lane, Uxbridge, UB8 3PH, UK; Department of Biomedical Engineering, CARIM School for Cardiovascular Diseases, Maastricht University, 6229 ER, the Netherlands.
Brunel Institute for Bioengineering, Brunel University London, Kingston Lane, Uxbridge, UB8 3PH, UK; British Heart Foundation Centre, King's College London, Strand, London, WC2R 2LS, UK.
J Mech Behav Biomed Mater. 2022 Oct;134:105339. doi: 10.1016/j.jmbbm.2022.105339. Epub 2022 Jul 4.
Age-related remodelling of the arterial wall shifts the load bearing from the compliant elastin network to the stiffer collagen fibres. While this phenomenon has been widely investigated in animal models, human studies are lacking due to shortage of donors' arteries. This work aimed to characterise the effect of ageing on the mechanical properties of the human aortic wall in the circumferential direction. N = 127 thoracic aortic rings (age 18-81 years) were subjected to circumferential tensile testing. The tangential elastic modulus (K) was calculated at pressure-equivalent stresses ranging 60-100 mmHg. Further, the mechanical data were fitted using the Holzpafel-Gasser-Ogden hyperelastic strain energy function (HGO-SEF), modelling the superimposed response of an isotropic matrix (elastin) reinforced by collagen fibres. K increased with age across at all considered pressures (p < 0.001), although more strongly at higher pressures. Indeed, the slope of the linear K-pressure relationship increased by 300% from donors <30 to ≥70 years (4.72± 2.95 to 19.06± 6.82 kPa/mmHg, p < 0.001). The HGO-SEF elastin stiffness-like parameter dropped by 31% between 30 and 40 years (p < 0.05) with non-significant changes thereafter. Conversely, changes in HGO-SEF collagen parameters were observed later at age>60 years, with the exponential constant increasing by ∼20-50 times in the investigated age range (p < 0.001). The results provided evidence that the human thoracic aorta undergoes stiffening during its life-course. Constitutive modelling suggested that these changes in arterial mechanics are related to the different degeneration time-courses of elastin and collagen; likely due to considerable fragmentation of elastin first, with the load bearing shifting from the compliant elastin to the stiffer collagen fibres. This process leads to a gradual impairment of the aortic elastic function with age.
随着年龄的增长，动脉壁会发生重塑，其负载从有弹性的弹性蛋白网络转移到更硬的胶原纤维上。虽然这一现象在动物模型中得到了广泛的研究，但由于供体动脉的缺乏，人类研究还很缺乏。本研究旨在描述年龄对人体主动脉壁环向力学性能的影响。共对 127 个胸主动脉环（年龄 18-81 岁）进行了环向拉伸试验。在等效压力为 60-100mmHg 的范围内计算切线弹性模量（K）。此外，通过 Holzpafel-Gasser-Ogden 超弹性应变能函数（HGO-SEF）对力学数据进行拟合，该模型模拟了由胶原纤维增强的各向同性基质（弹性蛋白）的叠加响应。结果表明，在所有考虑的压力下，K 随年龄的增加而增加（p<0.001），但在较高压力下增加更明显。实际上，从<30 岁到≥70 岁供体的 K-压力线性关系斜率增加了 300%（4.72±2.95 至 19.06±6.82kPa/mmHg，p<0.001）。HGO-SEF 中弹性蛋白刚度样参数在 30-40 岁之间下降了 31%（p<0.05），之后没有明显变化。相反，胶原参数的变化在>60 岁时才出现，在所研究的年龄范围内，指数常数增加了 20-50 倍（p<0.001）。研究结果表明，人体胸主动脉在其生命过程中会变硬。本研究的组成模型表明，动脉力学的这些变化与弹性蛋白和胶原的不同退变时间过程有关；可能是由于弹性蛋白首先发生了大量的碎片化，从而使负载从有弹性的弹性蛋白转移到更硬的胶原纤维上。随着年龄的增长，这一过程会导致主动脉弹性功能逐渐受损。
