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Competent elastic fibers endow central arteries with the compliance and resilience that are fundamental to their primary mechanical function in vertebrates. That is, by enabling elastic energy to be stored in the arterial wall during systole and then to be used to work on the blood during diastole, elastic fibers decrease ventricular workload and augment blood flow in pulsatile systems. Indeed, because elastic fibers are formed during development and stretched during somatic growth, their continual tendency to recoil contributes to the undulation of the stiffer collagen fibers, which facilitates further the overall compliance of the wall under physiologic pressures while allowing the collagen to limit over-distension during acute increases in blood pressure. In this paper, we use consistent methods of measurement and quantification to compare the biaxial material stiffness, structural stiffness, and energy storage capacity of murine common carotid arteries having graded degrees of elastic fiber integrity – normal, elastin-deficient, fibrillin-1 deficient, fibulin-5 null, and elastase-treated. The finding that the intrinsic material stiffness tends to be maintained nearly constant suggests that intramural cells seek to maintain a favorable micromechanical environment in which to function. Nevertheless, a loss of elastic energy storage capability due to the loss of elastic fiber integrity severely compromises the primary function of these central arteries. [ABSTRACT FROM AUTHOR]

Abstract: Arteries exhibit a remarkable ability to adapt to diverse genetic defects and sustained alterations in mechanical loading. For example, changes in blood flow induced wall shear stress tend to control arterial caliber and changes in blood pressure induced circumferential wall stress tend to control wall thickness. We submit, however, that the axial component of wall stress plays a similarly fundamental role in controlling arterial geometry, structure, and function, that is, compensatory adaptations. This observation comes from a review of findings reported in the literature and a comparison of four recent studies from our laboratory that quantified changes in the biaxial mechanical properties of mouse carotid arteries in cases of altered cell-matrix interactions, extracellular matrix composition, blood pressure, or axial extension. There is, therefore, a pressing need to include the fundamental role of axial wall stress in conceptual and theoretical models of arterial growth and remodeling and, consequently, there is a need for increased attention to evolving biaxial mechanical properties in cases of altered genetics and mechanical stimuli. [Copyright &y& Elsevier]

Abstract: Intraluminal exposure of the infrarenal aorta to porcine pancreatic elastase represents one of the most commonly used experimental models of the development and progression of abdominal aortic aneurysms. Morphological and histological effects of elastase on the aortic wall have been well documented in multiple rodent models, but there has been little attention to the associated effects on mechanical properties. In this paper, we present the first biaxial mechanical data on, and associated nonlinear constitutive descriptors of, the effects of elastase on the infrarenal aorta in mice. Quantification of the dramatic, acute effects of elastase on wall behavior in vitro is an essential first step toward understanding the growth and remodeling of aneurysms in vivo, which depends on both the initial changes in the mechanics and the subsequent inflammation-mediated turnover of cells and extracellular matrix that contributes to the evolving mechanics. [Copyright &y& Elsevier]

Elastic and muscular arteries are distinguished by their distinct microstructures, biomechanical properties, and smooth muscle cell contractile functions. They also exhibit differential remodeling in aging and hypertension. Although regional differences in biomechanical properties have been compared, few studies have quantified biaxial differences in response to hypertension. Here, we contrast passive and active changes in large elastic and medium- and small-sized muscular arteries in adult mice in response to chronic infusion of angiotensin over 14 days. We found a significant increase in wall thickness, both medial and adventitial, in the descending thoracic aorta that associated with trends of an increased collagen:elastin ratio. There was adventitial thickening in the small-sized mesenteric artery, but also significant changes in elastic lamellar structure and contractility. An increased contractile response to phenylephrine coupled with a reduced vasodilatory response to acetylcholine in the mesenteric artery suggested an increased contractile state in response to hypertension. Overall reductions in the calculated gradients in pulse wave velocity and elastin energy storage capability from elastic-to-muscular arteries suggested a possible transfer of excessive pulsatile energy into the small-sized muscular arteries resulting in significant functional consequences in response to hypertension. [ABSTRACT FROM AUTHOR]

Abstract: Cigarette smoking is the leading self-inflicted risk factor for cardiovascular diseases; it causes arterial stiffening with serious sequelea including atherosclerosis and abdominal aortic aneurysms. This work presents a new interpretation of arterial stiffening caused by smoking based on data published for rat pulmonary arteries. A structurally motivated “four fiber family” constitutive relation was used to fit the available biaxial data and associated best-fit values of material parameters were estimated using multivariate nonlinear regression. Results suggested that arterial stiffening caused by smoking was reflected by consistent increase in an elastin-associated parameter and moreover by marked increase in the collagen-associated parameters. That is, we suggest that arterial stiffening due to cigarette smoking appears to be isotropic, which may allow simpler phenomenological models to capture these effects using a single stiffening parameter similar to the approach in isotropic continuum damage mechanics. There is a pressing need, however, for more detailed histological information coupled with more complete biaxial mechanical data for a broader range of systemic arteries. [Copyright &y& Elsevier]