No abstract

No abstract

Guided by the experimental observations in the literature, this paper discusses two possible modes of defect growth in soft solids for which the size-dependent fracture mechanics is not always applicable. One is omni-directional growth, in which the cavity expands irreversibly in all directions; and the other is localized cracking along a plane. A characteristic material length is introduced, which may shed light on the dominant growth mode for defects of different sizes. To help determine the associated material properties from experimental measurement, the driving force of defect growth as a function of the remote load is calculated for both modes accordingly. Consequently, one may relate the measured critical load to the critical driving force and eventually to the associated material parameters. For comprehensiveness, the calculations here cover a class of hyperelastic materials. As an application of the proposed hypothesis, the experimental results (Cristiano et al., 2010, “An Experimental Investigation of Fracture by Cavitation of Model Elastomeric Networks,” J. Polym. Sci. Part B: Polym. Phys., 48(13), pp. 1409–1422) from two polymers with long and short chain elastomeric network are examined. The two polymers seem to be susceptible to either of the two dominating modes, respectively. The results are interpreted, and the material characteristic length and other growth parameters are determined.

No abstract

A computational framework is developed to consider the concurrent growth and remodelling (G&R) processes occurring in the large pulmonary artery (PA) and right ventricle (RV), as well as ventricular–vascular interactions during the progression of pulmonary arterial hypertension (PAH). This computational framework couples the RV and the proximal PA in a closed-loop circulatory system that operates in a short timescale of a cardiac cycle, and evolves over a long timescale due to G&R processes in the PA and RV. The framework predicts changes in haemodynamics (e.g. 68.2% increase in mean PA pressure), RV geometry (e.g. 38% increase in RV end-diastolic volume) and PA tissue microstructure (e.g. 90% increase in collagen mass) that are consistent with clinical and experimental measurements of PAH. The framework also predicts that a reduction in RV contractility is associated with long-term RV chamber dilation, a common biomarker observed in the late-stage PAH. Sensitivity analyses on the G&R rate constants show that large PA stiffening (both short and long term) is affected by RV remodelling more than the reverse. This framework can serve as a foundation for the future development of a more predictive and comprehensive cardiovascular G&R model with realistic heart and vascular geometries.