Frequency response of the arterial wall

The high frequency response of human common iliac arterial segments in vitro was investigated. It was found that at those high frequencies the response resembles that of a second order underdamped system. However, to simulate the arterial response throughout the frequency range, a higher order model is required. A fifth order system appears to describe the observed behaviour in a satisfactory way between 0.02 and 200 Hz.     

Plasminogen-activator of the arterial wall in occluded arteries

The plasminogen activator in 117 specimen of 20 coronary and 29 pulmonary arteries occluded completely by thrombi or emboli within the adventitia and intima was studied using TODD's histochemical method. 39 cadavers were used, 1--18 hours post mortem from subjects aged from 45 to 88 years. In occluded arteries both coronary and pulmonary the plasminogen activator activity was decreased in comparison with normal and atherosclerotic patients. In coronary and pulmonary arterial thrombi a low grade focal activity of plasminogen activator was detected. It is assumed that the decrease of plasminogen activator in the occluded human arterial wall is due to the impaired oxygen supply of the vessel wall and to the consumption of the plasminogen activator for thrombus lysis. These mechanisms are likely to influence the plasminogen activator for a certain and prolonged time, since there were no changes of fibrinolysis within the vessel wall of arteria carotis in rats where an acute thrombosis was elicited by means of an electric current.     

Isotropy and anisotropy of the arterial wall

The passive biomechanical response of intact cylindrical rat carotid arteries is studied in vitro and compared with the mechanical response of rubber tubes. Using true stress and natural strain in the definition of the incremental modulus of elasticity, the tissue wall properties are analyzed over wide ranges of simultaneous circumferential and longitudinal deformations. The type of loading chosen is 'physiological' i.e. symmetric: the cylindrical segments are subjected to internal pressure and axial prestretch without torsion or shear. Several aspects pertaining to the choice of parameters characterizing the material are discussed and the analysis pertaining to the deformational behavior of a hypothetical compliant tube with Hookean wall material is presented. The experimental results show that while rubber response can be adequately represented as linearly elastic and isotropic, the overall response of vascular tissue is highly non-linear and anisotropic. However, for states of deformation that occur in vivo, the elasticity of arteries is quite similar to that of rubber tubes and as such the arterial wall may be viewed as incrementally isotropic for the range of deformations that occur in vivo.     

Compressibility of arterial wall in ring-cutting experiments

It is common practice in the arterial wall modeling to assume material incompressibility. This assumption is driven by the observation of the global volume preservation of the artery specimens in some mechanical loading experiments. The global volume preservation, however, does not necessarily imply the local volume preservation - incompressibility. In this work, we suggest to use the arterial ring- cutting experiments for the assessment of the local incompressibility assumption. The idea is to track the local stretches of the marked segments of the arterial ring after the stress-relieving cut. In the particular case of the rabbit thoracic artery, considered in this work, the following criteria for radial stretches come from preliminary analysis. If after the radial cut the marked segments shorten at the inner surface of the wall and lengthen at the outer surface while remaining unchanged in the middle of the wall then material is locally incompressible. If, however, the marked segments remain unchanged at the surfaces while lengthening in the middle of the wall then the material is locally compressible. Any other scenario would be an indication of the improper modeling assumptions, i.e. residual stresses are not relieved or material constants are inaccurate etc. It is believed that the proposed approach can be successfully implemented in experiments shedding new light on the arterial incompressibility issue.     

Low-density lipoprotein binding affinity of arterial wall proteoglycans: characteristics of a chondroitin sulfate proteoglycan subfraction

The characteristics of an arterial wall chondroitin sulfate proteoglycan (CS-PG) subfraction that binds avidly to low-density lipoproteins (LDL) was studied. A large CS-PG was extracted from bovine aorta intima-media under dissociative conditions, purified by density-gradient centrifugation and gel filtration chromatography, and further subfractionated by affinity chromatography on LDL-agarose. A proteoglycan subfraction, representing 25% of the CS-PG, showed an elution profile (with dissociation from LDL-agarose occurring between 0.5 and 1.0 M NaCl) corresponding to that of heparin, heretofore considered to be the most strongly binding glycosaminoglycan with LDL. The proteoglycan subfraction which migrated as a single band on composite agarose-polyacrylamide gel electrophoresis contained chondroitin 6-sulfate, chondroitin 4-sulfate and dermatan sulfate in a proportion of 70:22:8. The core protein of the proteoglycan had an apparent molecular weight of 245,000, and contained approx. 33 glycosaminoglycan chains with an average molecular weight of 32,000. The CS-PG subfraction, like heparin, formed insoluble complexes in the presence of 30 mM Ca2+. Complexing of LDL with proteoglycan resulted in two classes of interactions with 0.1 and 0.3 proteoglycan monomer bound per LDL particle characterized by an apparent Kd of 4 and 21 nM, respectively. This indicates that multiple LDL particles bind to single proteoglycan monomers even at saturation. In contrast, LDL-heparin interactions showed a major component characterized by an apparent Kd of 151 nM and a Bmax of 9 heparin molecules per LDL particle. The occurrence of a potent LDL-binding proteoglycan subfraction within the family of arterial CS-PG may be of importance in terms of lipid accumulation in atherogenesis.     

An object-oriented modelling framework for the arterial wall

An object-oriented modelling framework for the arterial wall is presented. The novelty of the framework is the possibility to generate customisable artery models, taking advantage of imaging technology. In our knowledge, this is the first object-oriented modelling framework for the arterial wall. Existing models do not allow close structural mapping with arterial microstructure as in the object-oriented framework. In the implemented model, passive behaviour of the arterial wall was considered and the tunica adventitia was the objective system. As verification, a model of an arterial segment was generated. In order to simulate its deformation, a matrix structural mechanics simulator was implemented. Two simulations were conducted, one for an axial loading test and other for a pressure–volume test. Each simulation began with a sensitivity analysis in order to determinate the best parameter combination and to compare the results with analogue controls. In both cases, the simulated results closely reproduced qualitatively and quantitatively the analogue control plots.     

Measurement of wall motion and wall shear in a compliant arterial cast

Initial measurements of the time-varying wall shear rate at two sites in a compliant cast of a human aortic bifurcation are presented. The shear rates were derived from flow velocities measured by laser Doppler velocimetry (LDV) near the moving walls of the cast. To derive these shear rate values, the distance from the velocimeter sampling volume to the cast wall must be known. The time variation of this distance was obtained from LDV measurements of the velocity of the wall itself.     

Factors influencing the nonuniform localization of monocytes in the arterial wall

Adhesion of monocytes to arterial endothelium may contribute to the asymmetric distribution of atherosclerotic lesions. Possible mechanisms for adhesion in the relatively high shear stress environment found in arteries include greater monocyte deformation and/or more frequent penetration of microvilli through steric and charge barriers. In vivo, secondary flows generate forces acting normal to the endothelial cell surface. These forces may cause compression of the microvilli or enable cells to overcome steric or electrostatic barriers, increasing adhesion. To investigate this, we examined monocyte adhesion to activated endothelium in recirculating flow. Adhesion was characterized by short arrests in a narrow region on either side of the reattachment line. The median arrest time was longer than that observed at comparable shear stresses in a linear shear flow. The lifetimes of adhesion were analyzed using a model for multiple bond formation. For cells adhering near the reattachment line, the bond number per cell was greater than the value found for similar shear stresses under shear flow. Thus, multiple bond formation arising from greater normal forces in recirculating flow permits monocytes to adhere at higher shear stresses.     

Factors influencing arterial wall mass transport

Arterial wall mass transport has particularly attracted attention because it may be implicated in the development of arterial disease, including arteriosclerosis. A short review is presented of the structure of the arterial wall and of studies of mass transport within it. Recent findings confirm that mass transport occurs across the entire arterial wall apparently from the lumen to the adventitial lymphatics. Evidence has emerged of inhomogeneity of the distribution volume for extracellular tracers in different layers of the wall. An attempt is made to interpret results which indicate that distension per se of arteries and increase of medial smooth muscle tone tend to compact the medial interstitium whereas pressure driven convection across the wall tends to expand that tissue. These findings imply a potentially important role of endothelial permeability, smooth muscle tone and luminal pressure in influencing solute transport in the wall and wall transport properties.     

Radial construction of an arterial wall

Some of the most serious diseases involve altered size and structure of the arterial wall. Elucidating how arterial walls are built could aid understanding of these diseases, but little is known about how concentric layers of muscle cells and the outer adventitial layer are assembled and patterned around endothelial tubes. Using histochemical, clonal, and genetic analysis in mice, here we show that the pulmonary artery wall is constructed radially, from the inside out, by two separate but coordinated processes. One is sequential induction of successive cell layers from surrounding mesenchyme. The other is controlled invasion of outer layers by inner layer cells through developmentally regulated cell reorientation and radial migration. We propose that a radial signal gradient controls these processes and provide?evidence that PDGF-B and at least one other signal contribute. Modulation of such radial signaling pathways may underlie vessel-specific differences and pathological changes in arterial wall size and structure. VIDEO ABSTRACT: