Abstract

The thickening of the aortic wall is a mechanical adaptation to the prolonged increase in intravascular pressure resulting from hypertension, which is regulated by the smooth muscle cell layer (SML) and the elastic lamina (EL). Herein, we built a simplified computational model of the aortic media composed of SML and EL and simulated the phenomenon of EL undulation or EL buckling at no-load condition (in vitro) by releasing compressive prestress assigned to the EL. Using the design of experiments approach, we found that the prestress assigned to the EL, the thickness of the EL, and a coupled or interspace connecting length between the SML and the EL are significantly influential factors in representing EL buckling at the unloaded state. We also found that the degree of EL waviness and the change in residual stresses within the SML and the EL are inversely correlated. Furthermore, by increasing the stiffness of the SML, we successfully reconstructed the disappearance of EL undulation at 25% stretch, replicating the dilation of a normal aorta under physiological loading conditions. It can be expected that these findings will help unveil the roles of the SML and the EL in maintaining the mechanical homeostasis of the arterial wall.

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