In this paper we develop a new constitutive law for the description of the (passive) mechanical response of arterial tissue. The artery is modeled as a thick-walled nonlinearly elastic circular cylindrical tube consisting of two layers corresponding to the media and adventitia (the solid mechanically relevant layers in healthy tissue). Each layer is treated as a fiber-reinforced material with the fibers corresponding to the collagenous component of the material and symmetrically disposed with respect to the cylinder axis. The resulting constitutive law is orthotropic in each layer. Fiber orientations obtained from a statistical analysis of histological sections from each arterial layer are used. A specific form of the law, which requires only three material parameters for each layer, is used to study the response of an artery under combined axial extension, inflation and torsion. The characteristic and very important residual stress in an artery in vitro is accounted for by assuming that the natural (unstressed and unstrained) configuration of the material corresponds to an open sector of a tube, which is then closed by an initial bending to form a load-free, but stressed, circular cylindrical configuration prior to application of the extension, inflation and torsion. The effect of residual stress on the stress distribution through the deformed arterial wall in the physiological state is examined. The model is fitted to available data on arteries and its predictions are assessed for the considered combined loadings. It is explained how the new model is designed to avoid certain mechanical, mathematical and computational deficiencies evident in currently available phenomenological models. A critical review of these models is provided by way of background to the development of the new model.

https://hal.archives-ouvertes.fr/hal-01297725/document

A new constitutive framework for arterial wall mechanics and a comparative study of material models

http://biomechanics.stanford.edu/me338/me338_project04.pdf

Stress-dependent finite growth in soft elastic tissues

Cartilage and diarthrodial joints as paradigms for hierarchical materials and structures

An important factor in the transition from an open to a closed circulatory system was a change in vessel wall structure and composition that enabled the large arteries to store and release energy during the cardiac cycle. The component of the arterial wall in vertebrates that accounts for these properties is the elastic fiber network organized by medial smooth muscle. Beginning with the onset of pulsatile blood flow in the developing aorta, smooth muscle cells in the vessel wall produce a complex extracellular matrix (ECM) that will ultimately define the mechanical properties that are critical for proper function of the adult vascular system. This review discusses the structural ECM proteins in the vertebrate aortic wall and will explore how the choice of ECM components has changed through evolution as the cardiovascular system became more advanced and pulse pressure increased. By correlating vessel mechanics with physiological blood pressure across animal species and in mice with altered vessel compliance, we show that cardiac and vascular development are physiologically coupled, and we provide evidence for a universal elastic modulus that controls the parameters of ECM deposition in vessel wall development. We also discuss mechanical models that can be used to design better tissue-engineered vessels and to test the efficacy of clinical treatments.

/pdf/vascular-extracellular-matrix-and-arterial-mechanics-5bnvmr10by.pdf

Vascular Extracellular Matrix and Arterial Mechanics

Mechanical properties of the adventitia are largely determined by the organization of collagen fibers. Measurements on the waviness and orientation of collagen, particularly at the zero-stress state, are necessary to relate the structural organization of collagen to the mechanical response of the adventitia. Using the fluorescence collagen marker CNA38-OG488 and confocal laser scanning microscopy, we imaged collagen fibers in the adventitia of rabbit common carotid arteries ex vivo. The arteries were cut open along their longitudinal axes to get the zero-stress state. We used semi-manual and automatic techniques to measure parameters related to the waviness and orientation of fibers. Our results showed that the straightness parameter (defined as the ratio between the distances of endpoints of a fiber to its length) was distributed with a beta distribution (mean value 0.72, variance 0.028) and did not depend on the mean angle orientation of fibers. Local angular density distributions revealed four axially symmetric families of fibers with mean directions of 0°, 90°, 43° and −43°, with respect to the axial direction of the artery, and corresponding circular standard deviations of 40°, 47°, 37° and 37°. The distribution of local orientations was shifted to the circumferential direction when measured in arteries at the zero-load state (intact), as compared to arteries at the zero-stress state (cut-open). Information on collagen fiber waviness and orientation, such as obtained in this study, could be used to develop structural models of the adventitia, providing better means for analyzing and understanding the mechanical properties of vascular wall.

/pdf/experimental-investigation-of-collagen-waviness-and-35sv8tu15v.pdf

Experimental investigation of collagen waviness and orientation in the arterial adventitia using confocal laser scanning microscopy.

Tortuous arteries and veins are commonly observed in humans and animals. While mild tortuosity is asymptomatic, severe tortuosity can lead to ischemic attack in distal organs. Clinical observations have linked tortuous arteries and veins with aging, atherosclerosis, hypertension, genetic defects and diabetes mellitus. However, the mechanisms of their formation and development are poorly understood. This review summarizes the current clinical and biomechanical studies on the initiation, development and treatment of tortuous blood vessels. We submit a new hypothesis that mechanical instability and remodeling could be mechanisms for the initiation and development of these tortuous vessels.

/pdf/twisted-blood-vessels-symptoms-etiology-and-biomechanical-r2amht2di0.pdf

Twisted Blood Vessels: Symptoms, Etiology and Biomechanical Mechanisms

Rationale:Matrix metalloproteinase (MMP)-28 regulates the inflammatory and extracellular matrix responses in cardiac aging, but the roles of MMP-28 after myocardial infarction (MI) have not been explored. Objective:To determine the impact of MMP-28 deletion on post-MI remodeling of the left ventricle (LV). Methods and Results:Adult C57BL/6J wild-type (n=76) and MMP null (MMP-28−/−, n=86) mice of both sexes were subjected to permanent coronary artery ligation to create MI. MMP-28 expression decreased post-MI, and its cell source shifted from myocytes to macrophages. MMP-28 deletion increased day 7 mortality because of increased cardiac rupture post-MI. MMP-28−/− mice exhibited larger LV volumes, worse LV dysfunction, a worse LV remodeling index, and increased lung edema. Plasma MMP-9 levels were unchanged in the MMP-28−/− mice but increased in wild-type mice at day 7 post-MI. The mRNA levels of inflammatory and extracellular matrix proteins were attenuated in the infarct regions of MMP-28−/− mice, indicati...

/pdf/matrix-metalloproteinase-28-deletion-exacerbates-cardiac-2vgvjudtf0.pdf

Matrix Metalloproteinase-28 Deletion Exacerbates Cardiac Dysfunction and Rupture After Myocardial Infarction in Mice by Inhibiting M2 Macrophage Activation

Hai Chao Han

Papers

Twisted Blood Vessels: Symptoms, Etiology and Biomechanical Mechanisms

Matrix Metalloproteinase-28 Deletion Exacerbates Cardiac Dysfunction and Rupture After Myocardial Infarction in Mice by Inhibiting M2 Macrophage Activation

Longitudinal strain of canine and porcine aortas

Age-related cardiac muscle sarcopenia: Combining experimental and mathematical modeling to identify mechanisms.

A biomechanical model of artery buckling