Molecular-level collagen damage explains softening and failure of arterial tissues: A quantitative interpretation of CHP data with a novel elasto-damage model.

The present experimental-modelling study provides a quantitative interpretation of mechanical data and damage measurements obtained from collagen hybridizing peptide (CHP) techniques on overstretched sheep cerebral arterial tissues. To this aim, a structurally-motivated constitutive model is developed in the framework of continuum damage mechanics. The model includes two internal variables for describing the effects of collagen triple-helical unfolding via interstrand delamination: one governs plastic mechanisms in collagen fibers, leading to a stress softening response of the tissue at the macroscale; the other one describes the loss of fiber structural integrity, leading to tissue final failure. The proposed model is calibrated using the obtained mechanical experimental data, showing excellent fitting capabilities. The predicted evolution of internal variables agree well with independent measurements of molecular-level CHP-based damage data, obtaining an independent a posteriori validation of damage predictions. Moreover, available data on inelastic tissue elongation following supraphysiological loads are successfully reproduced. These outcomes further the hypothesis that the accumulation of interstrand delamination is a primary cause for the evolution of inelastic mechanisms in tissues, and in particular of stress softening up to failure.