Role of elastin and collagen in the passive mechanics of the circulatory system

The efficient transport of oxygenated blood via arteries is critical for normal functioning of an organism. The material properties and architecture of arteries are well adapted to endure the continuous, pulsatile blood flow over long periods of time. Mechanical properties of arteries are mainly determined by its active and passive components. In this thesis, I focus on the individual roles of passive components, elastin and collagen, in determining the mechanics of composite arterial walls.;To study how changes in the relative content of elastin and collagen alter vessel architecture and material properties, I treated individual arterial components with the enzymes, elastase and collagenase, which selectively degrade elastin and collagen respectively. I used equibiaxial mechanical tests to measure the resultant changes in arterial mechanics, histology to study the resulting architecture and assessed the collagen content using biochemical methods. Collagenase treatment increased the compliance of the tissue, whereas elastase treatment increased tissue stiffness. Further, results from the study suggest that collagen contributes to tissue anisotropy whereas elastin distributes tensile stresses in arteries.;Using a rigorous theoretical framework to guide experiments, I evaluated the constitutive properties of the elastin network isolated from arterial walls. Equibiaxial tests showed an equal stiffness in circumferential and axial directions for autoclaved elastin, suggesting an equal elastin crosslink density in these directions. However, the constitutive properties of elastin could not be accurately modeled using an isotropic Mooney-Rivlin form of the strain energy function. Using histological information, I proposed a novel constitutive model for the elastic network.;Normal vessel structure may get altered due to aging, hypertension and diseases. These changes alter the mechanical properties of the walls, requiring surgical and/or pharmacological interventions. The methods developed in these studies are well suited to study the effect of arterial diseases on its mechanics. As a case study, I focused on healing heart aneurysms in an ovine model over an eight month period. These are the only ex vivo mechanical, histological and biochemical data on such tissues and demonstrate how the evolving architecture and compositions affect tissue material properties. I hope these data will aid research on the cause, treatment and management of arterial diseases and provide useful mechanical and structural information for engineering tissue replacements.