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.     

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.     

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.     

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:     

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.     

Biomechanics of the venous wall under simulated arterial conditions

The failure of vein graft conduits implanted in the arterial circulation has been hypothesized to occur in part due to the exposure of the graft to altered biomechanical and fluid shearing forces. In the present study, these forces are characterized for canine internal jugular veins (IJV) exposed to realistic arterial flow dynamics. Freshly excised vein segments were mounted into a pulsatile perfusion apparatus and exposed to arterial flow conditions (P = 115/75 mmHg and Q = 110 ml min-1) for 2 h. Dynamic measurements of intraluminal pressure and flow rate and vessel wall radial distension were acquired to accurately quantitate the incremental modulus of elasticity; hoop, axial and radial wall stresses; and fluid shearing forces within the vessel. Identical measurements were performed on canine carotid arteries (CCA) to serve as a comparison. Under arterial conditions, IJV segments demonstrated a significant elevation (p less than 0.05) over the CCA in the incremental elasticity modulus, along with a corresponding elevation in hoop and axial wall stresses. Additionally the average wall shearing rate to which the IJV endothelial surface was exposed was a factor of six less than that observed in the CCA. These results are discussed in relationship to the clinical situation of vein graft adaptation to arterial hemodynamics.     

CO2-laser radiation damage of the arterial wall

This study describes the effects of CO2 laser radiation on the histology of the normal rabbit arterial wall, using models that simulate laser angioplasty and anastomosis. Rabbit arteries were exposed to laser treatments similar to those used clinically; 40, 0.5 sec pulses of 40-60 mW, CO2 continuous wavelength laser, or a 1/2-circumferential laser anastomosis with a 60-80 mW continuous pulse. Aneurysms developed in 8 of 22 femoral, 1 of 22 carotid, and no controls at 12 week. There were small breaks in the internal elastic lamina with atrophy, loss of muscularis, "packing" of the elastica, thinning of the muscularis at the damage site, and enlargement of the arterial diameter. Aneurysms developed in one femoral and no carotid anastomosed artery. Laser anastomoses demonstrated more muscle damage and loss, with extensive scarring and a wider area of elastic loss than the controls. The intima was reestablished with focal reduplication of the internal elastic lamina. There were no histologic differences between the arteries which developed aneurysms and those which did not in either series. These results suggest that low power laser damage of the arterial wall consists mainly of destruction of the muscularis propria, with minimal damage to the elastica.     

A semi-empirical nonlinear viscoelastic model of the arterial wall

A mathematical model was developed for the characterization of quasistatic nonlinear viscoelastic behaviour of large arteries with activated smooth muscle. Arteries were considered to belong to the class of viscoelastic materials with fading memory and the first order term of the integral polynomial constitutive equations of Pipkin and Rogers satisfying the nonlinear superposition principle was modified to handle responses to increasing and decreasing loads independently. The two creep functions contained by the obtained one dimensional constitutive equation were determined experimentally from the series of creep and recovery tests of increasing amplitude performed on isolated canine iliac arteries following the activation of the vascular smooth muscle by normal dose of norepinephrine in vitro. Utilizing the constitutive equation of the arterial wall and the tabulated values of creep functions successive stress-strain hysteresis loops of various constant stress rates were simulated by digital computer. The computed hysteresis loops demonstrated the main characteristics, such as the weak and asymmetric rate-sensitivity of the experimentally observed hysteresis of arteries qualitatively well, thus allowing certain conclusions on the mechanism of quasistatic viscoelastic behaviour of vascular smooth muscle.     

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.     

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.     

Effects of arterial wall stress on vasomotion

Smooth muscle and endothelial cells in the arterial wall are exposed to mechanical stress. Indeed blood flow induces intraluminal pressure variations and shear stress. An increase in pressure may induce a vessel contraction, a phenomenon known as the myogenic response. Many muscular vessels present vasomotion, i.e., rhythmic diameter oscillations caused by synchronous cytosolic calcium oscillations of the smooth muscle cells. Vasomotion has been shown to be modulated by pressure changes. To get a better understanding of the effect of stress and in particular pressure on vasomotion, we propose a model of a blood vessel describing the calcium dynamics in a coupled population of smooth muscle cells and endothelial cells and the consequent vessel diameter variations. We show that a rise in pressure increases the calcium concentration. This may either induce or abolish vasomotion, or increase its frequency depending on the initial conditions. In our model the myogenic response is less pronounced for large arteries than for small arteries and occurs at higher values of pressure if the wall thickness is increased. Our results are in agreement with experimental observations concerning a broad range of vessels.     

Metabolic heterogeneity of proteoglycans from arterial wall

• 1.1. Four pools of proteoglycans were isolated by sequential extraction from pig arterial wall. They exhibited great metabolic and chemical heterogeneity.
• 2.2. Proteoglycans extracted by 4 M guanidinium chloride showed the highest labeling rate; and among the different glycosaminoglycans chains, the highest incorporation was measured in heparan sulfate chains.
• 3.3. Pulse chase experiments gave some evidence of precursor product relation between insoluble or less soluble, intracellular proteoglycans and the other soluble proteoglycans of the matrix.