We developed a structure-based model of the arterial wall to explain the effect of dissolution of smooth muscle cells (SMC) on the mechanical behavior of the artery and to obtain a better understanding of the interaction between the different wall components. Pressure-radius curves and dimensions of zero-stress configuration were measured in 5 control and 5 decellularized porcine common carotid arteries. We found that 13% of elastin is associated with the smooth muscle cells (SMC) whereas the rest 87% is associated with the extracellular matrix (ECM). Further, we found that the elastin related to SMC and the one related to the ECM have circumferential prestretches of 2.04 and 0.89, respectively. We conclude that the majority of elastic in the media is linked to ECM and is under compression at zero load, whereas a minor part is linked to VSM and is under tension (SMC related) at its zero load state. Upon chemical dissolution of the muscle cells elastin in series with SMC do not bear load allowing elastin connected to ECM to release its compressive prestress, leading to the expansion of the artery.

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