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Strain-induced crystallization is a unique crystallization process taking place solely in polymers subjected to large deformations. It plays a major role for reinforcement and improvement of mechanical properties of polymers with a high regularity of the molecular structure. In this paper, we develop a micromechanical model for the strain-induced crystallization in filled rubbers. Accordingly, the strain-induced crystallization is considered as a process triggered by fully stretched and continued by semistretched polymer chains. The model extends the previously proposed network evolution model [Dargazany and Itskov, Int. J. Solids Struct. 46, 2967 (2009)] and can thus, in addition to the stress upturn and evolution of crystallinity, take into account several inelastic features of filled rubbers, such as the Mullins effect, permanent set, and induced anisotropy. Finally, the accuracy of the model is verified against different set of experimental data both with respect to the stress-strain and crystallization-strain relations. The model exhibits good agreement with the experimental results, which, besides its relative simplicity, makes it a good option for finite-element implementations.

Experimental and computational studies suggest a substantial variation in the mechanical responses and collagen fibre orientations of the two structurally important layers of the arterial wall. Some observe the adventitia to be an order of magnitude stiffer than the media whilst others claim the opposite. Furthermore, studies show that molecular metabolisms may differ substantially in each layer. Following a literature review that juxtaposes the differing layer-specific results we create a range of different hypothetical arteries: (1) with different elastic responses, (2) different fibre orientations, and (3) different metabolic activities during adaptation. We use a finite element model to investigate the effects of those on: (1) the stress response in homeostasis; (2) the time course of arterial adaptation; and (3) an acute increase in luminal pressure due to a stressful event and its influence on the likelihood of aneurysm rupture. Interestingly, for all hypothetical cases considered, we observe that the adventitia acts to protect the wall against rupture by keeping stresses in the media and adventitia below experimentally observed ultimate strength values. Significantly, this conclusion holds true in pathological conditions.

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