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The effect of pulse pressure on arterial wall remodeling has not been clearly defined. The objective of this study was to evaluate matrix remodeling in arteries under nonpulsatile and hyperpulsatile pressure as compared with arteries under normal pulsatile pressure. Porcine carotid arteries were cultured for 3 and 7 days under normal, nonpulsatile, and hyperpulsatile pressures with the same mean pressure and flow rate using an ex vivo organ culture model. Fenestrae in the internal elastic lamina, collagen, fibronectin, and gap junction protein connexin 43 were examined in these arteries using con focal microscopy, immunoblotting, and immunohistochemistry. Our results showed that after 7 clays, the mean fenestrae size and the area fraction of fenestrae decreased significantly in nonpulsatile arteries (51% and 45%, respectively) and hyperpulsatile arteries (45% and 54%, respectively) when compared with normal pulsatile arteries. Fibronectin decreased (29.9%) in nonpulsatile arteries after 3 days but showed no change after 7 days, while collagen 1 levels increased significantly (106%) in hyperpulsatile arteries after 7 days. The expression of connexin 43 increased by 35.3% in hyperpulsatile arteries after 7 days but showed no difference in nonpulsatile arteries. In conclusion, our results demonstrated, for the first time, that an increase or a decrease in pulse pressure from its normal physiologic level stimulates structural changes in the arterial wall matrix. However, hyperpulsatile pressure has a more pronounced effect than the diminished pulse pressure. This effect helps to explain the correlation between increasing wall stiffness and increasing pulse pressure in vivo. [DOI: 10.1115/1.3202785] Keywords: pulsatile pressure, internal elastic lamina, collagen, fibronectin, connexin 43, porcine artery, ex vivo, organ culture

Arterial axial strains, present in the in vivo environment, often become reduced due to either bypass grafting or the normal aging process. Since the prevalence of hypertension increases with aging, arteries are often exposed to both decreased axial stretch and increased transmural pressure. The combined effects of these mechanical stimuli on the mechanical properties of vessels have not previously been determined. Porcine carotid arteries were cultured for 9 days at normal and reduced axial stretch ratios in the presence of normotensive and hypertensive transmural pressures using ex vivo perfusion techniques. Measurements of the amount of axial stress were obtained through longitudinal tension tests while inflation-deflation test results were used to determine circumferential stresses and incremental moduli. Macroscopic changes in artery geometry and zero-stress state opening angles were measured. Arteries cultured ex vivo remodeled in response to the mechanical environment, resulting in changes in arterial dimensions of up to ~25% and changes in zero-stress opening angles of up to ~55[degrees]. While pressure primarily affected circumferential remodeling and axial stretch primarily affected axial remodeling, there were clear examples of interactions between these mechanical stimuli. Culture with hypertensive pressure, especially when coupled with reduced axial loading, resulted in a rightward shift in the pressure-diameter relationship relative to arteries cultured with normotensive pressure. The observed differences in the pressure-diameter curves for cultured arteries were due to changes in artery geometry and, in some cases, changes in the arteries' intrinsic mechanical properties. Relative to freshly isolated arteries, arteries cultured under mechanical conditions similar to in vivo conditions were stiffer, suggesting that aspects of the ex vivo culture other than the mechanical environment also influenced changes in the arteries' mechanical properties. These results confirm the well-known importance of transmural pressure with regard to arterial wall mechanics while highlighting additional roles for axial stretch in determining mechanical behavior. [DOI: 10.1115/1.3200910] Keywords: hypertension, organ culture, incremental modulus, pressure-diameter relationship

Computational models of arterial growth and remodeling promise to increase our understanding of basic biological processes, such as development, tissue maintenance, and aging, the biomechanics of functional adaptation, the progression and treatment of disease, responses to injuries, and even the design of improved replacement vessels and implanted medical devices. Ensuring reliability of and confidence in such models requires appropriate attention to verification and validation, including parameter sensitivity studies. In this paper, we classi different types of parameters within a constrained mature model of arterial growth and remodeling; we then evaluate the sensitivity of model predictions to parameter values that are not known directly from experiments ,for cases of modest sustained alterations in blood flow and pressure as well as increased axial extension. Particular attention is directed toward complementary roles of smooth muscle vasoactivity and matrix turnover, with an emphasis on mechanosensitive changes in the rates of turnover of intramural fibrillar collagen and smooth muscle in maturity. It is shown that vasoactive changes influence the rapid change in caliber that is needed to maintain wall shear stress near its homeostatic level and the longer term changes in wall thickness that are needed to maintain circumferential wall stress near its homeostatic target. Moreover, it is shown that competing effects of intramural and wall shear stress-regulated rates of turnover can develop complex coupled responses. Finally, results demonstrate that the sensitivity to parameter values depends upon the type of perturbation from normalcy, with changes in axial stretch being most sensitive consistent with empirical reports. [DOI: 10.1115/1.3192144] Keywords: vasoactivity, stress, collagen turnover, verification, experimental design

A distributed model of the human arterial tree including all main systemic arteries coupled to a heart model is developed. The one-dimensional (1-D) form of the momentum and continuity equations is solved numerically to obtain pressures and flows throughout the systemic arterial tree. Intimal shear is modeled using the Witzig-Womersley theory. A nonlinear viscoelastic constitutive law for the arterial wall is considered. The left ventricle is modeled using the varying elastance model. Distal vessels are terminated with three-element windkessels. Coronaries are modeled assuming a systolic flow impediment proportional to ventricular varying elastance. Arterial dimensions were taken from previous 1-D models and were extended to include a detailed description of cerebral vasculature. Elastic properties were taken from the literature. To validate model predictions, noninvasive measurements of pressure and flow were performed in young volunteers. Flow in large arteries was measured with MRI, cerebral flow with ultrasound Doppler, and pressure with tonometry. The resulting 1-D model is the most complete, because it encompasses all major segments of the arterial tree, accounts for ventricular-vascular interaction, and includes an improved description of shear stress and wall viscoelasticity. Model predictions at different arterial locations compared well with measured flow and pressure waves at the same anatomical points, reflecting the agreement in the general characteristics of the 'generic 1-D model' and the 'average subject' of our volunteer population. The study constitutes a first validation of the complete 1-D model using human pressure and flow data and supports the applicability of the 1-D model in the human circulation. wave propagation; heart model; cerebral circulation; ventricular-vascular coupling; nonlinear viscoelasticity; ultrasound; noninvasive vascular imaging

Problem statement: Modeling Human cardiovascular system was always an important issue from long past because by doing such modeling, investigation in cardiovascular system and its abnormities would be simpler. One of the most effective ways to do such modeling is using lumped method (Electrical analogy). Approach: Lumped method was used for simulating a complete model in this approach. A 36-vessel model was chosen to make equivalent circuit of lumped method from it. This complicated circuit includes equivalent segment for arteries, pulmonary, atrium, left and right ventricles. Furthermore, in this complex circuit some additional points were considered to improve this method. Some of the most important considerations to advance this modeling method was exact simulation of right and left ventricles pressures, division of ascending aorta, femoral carotid in respect into 27, 10, 31 segments and adding peristaltic motions of vessels in descending arteries (thoracic to femoral) as a further pressure supplier respect to ventricles. Results: As a result of these considerations the pressure graphs from our complex circuit in descending arteries were so close to real graphs from biological texts which were earned by advanced instruments. Conclusion: citation of current modeling would be verified strongly. Consequently obstruction in femoral and right common carotid was probed with this complicated circuit and its results were shown in this study. Key words: Electrical analogy (lumped method), cardiovascular systems, descending arteries, peristaltic motion of vessels walls, RLC circuit-obstruction, INTRODUCTION Human cardiovascular system health and its abnormities are so important for clinical researches. Because by knowing the influences of diseases on cardiovascular system properties such as pressure graph the [...]

Passive elastic behavior of arterial wall remains difficult to model. Although phenomenological and structural models exist, the question of how the three-dimensional network structure of the collagen in the artery determines its mechanical properties is still open. A model is presented that incorporates a collagen network as well as the noncollagenous material that comprise the artery. The collagen architecture is represented as a network of interconnected fibers, and a neo-Hookean constitutive equation is used to describe the contribution of the noncollagenous matrix. The model is multiscale in that volume-averaging theory is applied to the collagen network, and it is structural in that parameters of the microstructure of the collagen network were considered instead of a macroscopic constitutive law. The computational results provided a good fit to published experimental dam for decellularized porcine carotid arteries. The model predicted increased circumferential compliance for increased axial stretch, consistent with previously published reports, and a relatively small sensitivity to open angle. Even at large extensions, the model predicted that the noncollagenous matrix would be in compression, preventing collapse of the collagen network. The incorporation of fiber-fiber interactions led to an accurate model of artery wall behavior with relatively few parameters. The counterintuitive result that the noncollagenous component is in compression during extension and inflation of the tissue suggests that the collagen is important even at small strains, with the noncollagenous components supporting the network, but not resisting the load directly. More accurate representation of the microstructure of the artery wall is needed to explore this issue further. [DOI: 10.1115/1.2746387] Keywords: finite element method, collagen, elastin, network

Rabbit ear resistance artery vasomotion phase space portraits were used to derive iterative maps via the Poincare section. The vasomotion approximates the movement on the surface of a torus. In a quasiperiodic system, the strong coupling of two oscillators becomes locked into a rational ratio which can be used as the basis for a staircase function. Derivation of this function proves that frequency-locked states and the associated quasiperiodic transition to chaos conforms to an iterative circle map.

This study aimed to model phenomenologically the dynamics of arterial wall remodeling under hypertensive conditions. Sustained hypertension was simulated by a step increase in blood pressure. The arterial wall was considered to be a thick-walled tube made of nonlinear elastic incompressible material. Remodeling rate equations were postulated for the evolution of the geometric dimensions of the hypertensive artery at the zero-stress state, as well as for one of the material constants in the constitutive equations. The driving stimuli for the geometric adaptation are the normalized deviations of wall stresses from their values under normotensive conditions. The geometric dimensions are modulated by the evolution of the deformed inner radius, which serves to restore the level of the flow-induced shear stresses at the arterial endothelium. Mechanical adaptation is driven by the difference between the area compliance under hypertensive and normotensive conditions. The predicted time course of the geometry and mechanical properties of arterial wall are in good qualitative agreement with published experimental findings. The model predicts that the geometric adaptation maintains the stress distribution in arterial wall to its control level, while the mechanical adaptation restores the normal arterial function under induced hypertension.

The apex of human vertebro-basilar junctions can be sharp-edged or blunted. In the present study, the effect of a blunted apex on the flow in vertebro-basilar junction models is investigated. We compared the flow phenomena in a series of junction models with blunted apices and confluence angles 45, 85, and 125 deg with the flow phenomena in a series of junction models with sharp-edged apices and the same range of confluence angles, studied in a previous paper (Ravensbergen et al., 1996b). The blunting of the apex appears to have an effect on the size of the local recirculation area near the apex and the prevailing low velocities. Large recirculation areas are found in the models with blunted apices, especially in those with small confluence angles. In addition, the blunting of the apex has no influence on the flow further downstream, nor on the structure and strength of the secondary flow field. Furthermore, a blunted apex appears to be a geometric risk factor for atherosclerosis. This supports the hypotheses that recirculation areas and low wall shear stress influence the development of atherosclerotic plaques.

A fiber matrix model was developed for the analysis of the mechanisms that promote structural and hydraulic conductivity changes in an intact artery wall in the presence of transmural pressure. The fiber matrix model neglects nonuniform deformation of the endothelium due to the pressure variation in the intima to avoid complicated, nonlinear elastohydrodynamic interaction problems. Furthermore, two-dimensional model for filtration flow through fenestral pores considers the role played by the compaction of the arterial intima in modulating the total hydraulic conductivity in intact artery wall.

The incorporation of a pressure-dependent compliance in the three-element windkessel model (model A) of the systemic arterial system was evaluated to determine the accuracy of the linear model. Comparison of model A with nonlinear versions of the three-element windkessel model (model B1 and B2) indicated the improved data fit due to constant pressure-dependent compliance in model A. Furthermore, model A provided more accurate parameter estimates compared to models B1 and B2.

The bidirectional cavopulmonary anastomosis (BCPA or bidirectional Glenn) is an operation to treat congenital heart diseases of the right heart by diverting the systemic venous return from the superior vena cava to both lungs. The main goal is to provide the correct perfusion to both lungs avoiding an excessive increase in systemic venous pressure. One of the factors which can affect the clinical outcome of the surgically reconstructed circulation is the amount of pulsatile blood flow coming from the main pulmonary artery. The purpose of this work is to analyse the influence of this factor on the BCPA hemodynamics. A 3-D finite element model of the BCPA has been developed to reproduce the flow of the surgically reconstructed district. Geometry and hemodynamic data have been taken from angiocardiogram and catheterization reports, respectively. On the basis of the developed 3-D model, four simulations have been performed with increasing pulsatile blood flow rate from the main pulmonary artery. The results show that hemodynamics in the pulmonary arteries are greatly influenced by the amount of flow through the native main pulmonary artery and that the flow from the superior vena cava allows to have a similar distribution of the blood to both lungs, with a little predilection for the left side, in agreement with clinical postoperative data.

Axisymmetric laminar blood flows in a stenotic model vessel are calculated by using a finite-difference scheme of the Navier-Stokes equations. The wavy lumen are transformed to a rectangular region with fine and irregular meshes mapped to regular ones in the computational domain. The pulsating flow is controlled by a time-dependent yon Karman number. At the upstream and downstream ends, the local acceleration is employed to replace the Neumann boundary condition for solving the pressure field from the divergence of the Navier-Stokes equations, resulting in a new treatment on the inlet and outlet conditions for transient flow problems. The kinematic and dynamic characteristics of vortices in the pulsating flow processes are analyzed along with the pressure and shear fields.

Constrained constructive optimization was used to generate a model for a series of complex arterial trees by optimizing different target functions. Changes in the target function produced differing tree structure plus changing path length for blood transport, pressure and segment orientation. Computer simulation of blood flow resulted in some geometrically impossible fractal models.

The arterial media is modeled as a periodic array of cylindrical smooth muscle cells residing in a matrix comprised of proteoglycan and collagen fibers. Using Brinkman's model to describe transmural flow through such a fibrous media, we calculate the effective hydraulic permeability of the media and the wall shear stress on smooth muscle cells. Two interesting results are obtained: first, the wall shear stress on smooth muscle cells is on the order of 1 dyne/[cm.sup.2], which is in the range known to affect endothelial cells in vitro; second, the flow resistance due to smooth muscle cells is not negligible compared to the resistance due to the fiber matrix.

A new model is presented for the growth of cellular level macromolecular leakage spots in the arterial intima. The theoretical approach differs from the recent study by Yuan et al. in that it directly models and calculates the intimal transport parameters based on Frank and Fogelman's ultrastructural observations of the extracellular subendothelial proteoglycan matrix that their rapid freeze etching technique preserves. Using a heterogeneous fiber matrix theory, which includes proteoglycan and collagen components, the model predicts that the Darcy permeability [K.sub.p] and macromolecular diffusivity D of the subendothelial intima is two orders of magnitude larger than the corresponding values measured in the media, and supports the observations in Lark et al. that the proteoglycan structure of the intima differs greatly from that of the media. Numerical results show that convection parallel to the endothelium is a very significant transport mechanism for macromolecules in the intima in a large region of roughly 200 [[micro]meter] diameter surrounding the leaky cleft. The predictions of the new model for the early-time spread of the advancing convective-diffusive front from the leakage spots in the intima are in close agreement with our experimental measurements for the growth of HRP spots in [20]. The regions of high concentration surrounding the leaky cell, however, are much more limited and cover an area that is typically equivalent to 20 cells. This prediction is consistent with the recent measurements of Truskey et al. for LDL spot size in rabbit aorta and the hypothesis advanced in [19] that there is a colocalization of subendothelial liposome growth and cellular level leakage. Finally, comparison of predicted and experimentally-measured average LDL concentration in leakage spots strongly suggests that there is significant local molecular sieving at the interface between the fenestral openings in the internal elastic lamina and the media.

Open-loop experimental studies of the relationship between mean systemic arterial pressure (SAP) and mean baroreceptor pressure (BP) reveal that analytical data on SAP-BP and open loop gain (G)-BP curves derived from logistic function (LF) and normal-cumulative distribution function (CDF) are identical. Approximations of SAP-BP data using third-order polynomials have to be avoided for quantitative assay SAP-BP curves.

Arterial wall mechanics has been studied for nearly 200 years. This subject is of importance if we are to gain a fundamental understanding of this complex biological structure, as well as information needed to design prosthetics. Biomechanical arterial models continue to play an important role in the study of atherosclerosis, a disease of the arterial wall that is the chief cause of mortality and morbidity in the United States and the Western World. Over the past 20 years, the finite element model (FEM) has been used in a variety of ways to simulate the structural response of large arteries. Our purpose is to summarize the uses of FEMs in arterial mechanics. We will also indicate directions for future research in this area. A specialized FEM was described in the literature for the study of transport in the arterial wall, however the convection was not directly linked to arterial wall mechanics. In this paper special attention will be given to the development of FEMs based on the poroelastic view of arterial tissues which couple wall deformation, free tissue fluid motion, and associated transport phenomena in the arterial wall. In the future such models should provide fundamental quantitative information relating arterial wall mechanics and transport which may lead to a better understanding of both normal arterial physiology and atherogenesis.

The subclavian steal syndrome that affects the human artery system is studied using an elastic model. Experiments are carried out wherein simulated blood flow for cerebral distribution is generated at a constant Reynolds number by means of a motor-powered pulsatile device. Results reveal that a single occlusion is capable of producing a double steal syndrome at the brachiocephalic artery.