Vascular resistance

Summary

Vascular resistance is the resistance that must be overcome to push blood through the circulatory system and create blood flow. The resistance offered by the systemic circulation is known as the systemic vascular resistance (SVR) or may sometimes be called by the older term total peripheral resistance (TPR), while the resistance offered by the pulmonary circulation is known as the pulmonary vascular resistance (PVR). Systemic vascular resistance is used in calculations of blood pressure, blood flow, and cardiac function. Vasoconstriction (i.e., decrease in blood vessel diameter) increases SVR, whereas vasodilation (increase in diameter) decreases SVR. Units for measuring Units for measuring vascular resistance are dyn·s·cm−5, pascal seconds per cubic metre (Pa·s/m3) or, for ease of deriving it by pressure (measured in mmHg) and cardiac output (measured in L/min), it can be given in mmHg·min/L. This is numerically equivalent to hybrid resistance units (HRU), also known as Wood

Official source

https://en.wikipedia.org/wiki/Vascular_resistance

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Contribution of the Arterial System and the Heart to Blood Pressure during Normal Aging - A Simulation Study

Elira Maksuti, Nikolaos Stergiopulos, Nico Westerhof

During aging, systolic blood pressure continuously increases over time, whereas diastolic pressure first increases and then slightly decreases after middle age. These pressure changes are usually explained by changes of the arterial system alone (increase in arterial stiffness and vascular resistance). However, we hypothesise that the heart contributes to the age-related blood pressure progression as well. In the present study we quantified the blood pressure changes in normal aging by using a Windkessel model for the arterial system and the time-varying elastance model for the heart, and compared the simulation results with data from the Framingham Heart Study. Parameters representing arterial changes (resistance and stiffness) during aging were based on literature values, whereas parameters representing cardiac changes were computed through physiological rules (compensated hypertrophy and preservation of end-diastolic volume). When taking into account arterial changes only, the systolic and diastolic pressure did not agree well with the population data. Between 20 and 80 years, systolic pressure increased from 100 to 122 mmHg, and diastolic pressure decreased from 76 to 55 mmHg. When taking cardiac adaptations into account as well, systolic and diastolic pressure increased from 100 to 151 mmHg and decreased from 76 to 69 mmHg, respectively. Our results show that not only the arterial system, but also the heart, contributes to the changes in blood pressure during aging. The changes in arterial properties initiate a systolic pressure increase, which in turn initiates a cardiac remodelling process that further augments systolic pressure and mitigates the decrease in diastolic pressure.

Public Library of Science2016

Arterial in vitro remodeling

Gabriela Montorzi Thorell

Vascular remodeling is defined as any enduring change in the size and composition of an adult blood vessel, allowing adaptation or repair. The vascular remodeling response has been shown to depend on a variety of endogenous and environmental factors. Physiological remodeling is a tightly regulated process that mainly occurs in response to long-term changes in hemodynamic conditions. The adaptation to these hemodynamic changes implies the production of mediators that influence structure as well as function. A loss of regulation in the adaptive response underlies the pathogenesis of major cardiovascular diseases, including hypertension, atherosclerosis, restenosis and arterial aneurismal dilatation. Specialized enzymes called matrix metalloproteinases (MMPs) have been shown to have a predominant participation in the reorganization of the vessel structure, through the degradation of the extracellular matrix scaffold. The aim of this thesis is to gain insight in the biological and mechanical processes taking place in the vascular wall as an adaptive response to different biomechanical stimuli such as blood pressure and blood flow. This work proposes a new model for the study of vascular remodeling where physical factors acting on the arterial wall can be dissociated and analyzed, individually, in relation to the biological response. The results are presented in form of an introduction, three scientific papers and a conclusion section. The investigation has been designed around three different approaches: adaptation of a non-uniform artery to an in vitro environment, vascular adaptation to steady and pulsatile pressure and vascular adaptation to unidirectional and oscillatory flow. The adaptive response to each one of the variables chosen has been analyzed through biological and biomechanical remodeling indicators of the arterial wall. The introduction is an overview of the biological and biomechanical characteristics of arterial wall in relation to the remodeling process. The contribution of vascular smooth muscle cells and extracellular matrix to physiological and pathological arterial remodeling is discussed. Paper I assesses the relative remodeling of a non-axisymmetric artery in relation to its environment. The study considers the native circumferential asymmetry of the porcine right common carotid, which results from the non-homogenous mechanical and hemodynamic native environment. The adaptive response of the artery to an in vitro perfusion environment is analyzed. The study shows that in vitro perfusion leads, through remodeling, to a circumferentially uniform scleroprotein distribution and to a change in arterial compliance. This study emphasizes the link between structural changes, the biomechanical response and the enzymatic implication in the adaptive response. In paper II we investigate the role of continuous and cyclic stretch, produced by steady or pulsatile pressure acting on the arterial wall, on the remodeling response. The study shows that exposure to continuous and cyclic stretch differentially affects the relative scleroprotein content and leads to a change in arterial wall stiffness. The adaptive outcome is studied through an integrative approach taking into consideration the geometrical and structural adaptation, the biomechanical behavior and the enzymatic agents implicated in extracellular matrix turnover. Paper III analyzes the influence of different flow patterns on the arterial adaptive response. We investigate the differential effects of oscillatory flow, mimicking a plaque-prone hemodynamic environment, and unidirectional flow, to mimicking a physiologically protective (plaquefree) environment. The effect of these hemodynamic forces on the remodeling response are characterized through the study of endothelial and smooth muscle cell function as well as through assessment of agents influencing extracellular matrix turnover. The conclusions section presents a synthesis of the results and contribution of this thesis and proposes perspectives for future studies.

EPFL2004

This thesis contributes to the field of biomechanics of vascular wall. The focus is particularly on the microstructure of vascular elastin and collagen constituents and their contribution to the macroscopic mechanical behavior of the wall. The analysis is done in the framework of continuum mechanics. The work characterizes structural features of elastin and collagen fibers using microscopy techniques and introduces these features to constituent-based constitutive models. The models are applied to the experimental data, derived from inflation-extension tests, to predict the gross mechanical behavior of the tissue. The developed constitutive models could be further used to study in detail the mechanics of vascular tissue in health and disease. The thesis is presented in form of an introduction, four chapters (corresponding to four papers) and a conclusion. The introduction provides the motivation for this thesis as well as the background on vascular wall structure and mechanics. A brief description of the imaging techniques used is presented. Also, structural constitutive modeling of vascular wall is briefly discussed with particular attention to the modeling of elastin and collagen constituents. The first paper focuses on anisotropic properties of elastin in veins. We show that earlier constituent-based strain energy functions (SEFs), where elastin is modeled as an isotropic material, fail in describing accurately the tissue response to inflation-extension loading. We hypothesize that these shortcomings are partly due to unaccounted anisotropic properties of elastin. We extend the previously developed biomechanical model in our laboratory (Zulliger et al., 2004, J. Biomech., 37(7): 989-1000 (2004)) to account for elastin anisotropy and present an anisotropic strain energy function for elastin with one family of fibers in the longitudinal direction. The model is validated using experimental data from inflation-extension tests on rabbit facial veins. The tissue is tested under a fully relaxed smooth muscle state, for longitudinal stretch ratios ranging from 100% to 130% of the in vivo length. The model with the anisotropic elastin fits well the data for a wide range of longitudinal stretch ratios. The main finding of this paper is that the anisotropic description of elastin is required for a full 3-D characterization of the biomechanics of the venous wall. The second paper addresses the role of elastin in anisotropic properties of arteries with particular attention to the structural organization of elastin. A constituent-based model including an anisotropic elastin, with one family of fibers in the circumferential direction, is presented. Micro-structural imaging, based on electron microscopy techniques, is used to support this anisotropy. Inflationˆextension tests, on intact and elastase-treated arteries, provide a data set to validate the model and to study the effect of elastin removal. We show that the SEF, with an anisotropic elastin part, characterizes more accurately the mechanical properties of the arterial wall as compared to models with simply an isotropic elastin. Transmission electron microscopy (TEM) and serial block-face scanning electron microscopy (SBF-SEM) show interlamellar elastin fibers in the circumferential direction and therefore support the nature of the assumed anisotropy. The model predicts an earlier engagement of collagen in elastase-treated arteries compared to the intact arteries and thus suggests a clear functional interaction between the elastin and collagen component that is often neglected in constituent-based SEFs. The third paper presents a structural constitutive model of the vascular wall which integrates both waviness and orientational dispersion of collagen fibers. We extend the model of Zulliger et al., which already accounts for collagen waviness, to include orientational distribution of collagen. We study the effect of parameters related to the orientational distribution on macro-mechanical behavior of the tissue during inflation-extension tests. The model is further applied to the experimental data from rabbit facial veins. The model accurately fits the experimental data of veins, but it does not improve the quality of the fit compared to the one without dispersion. We show that the orientational dispersion of collagen fibers can be compensated by a less abrupt and shifted to higher strain collagen engagement pattern. This should be taken into consideration when the model is used to fit experimental data and model parameters are used to study structural modifications of collagen fiber network in physiology and disease. In the fourth paper, we measure and quantify the waviness and orientational distributions of collagen in rabbit carotids. Quantification of collagen orientation distributions at the zero stress state of arteries is needed to develop realistic and precise biomechanical models. Using the fluorescence collagen marker CNA38-OG488 and confocal laser scanning microscopy, we visualize collagen fibers in adventitia of rabbit common carotids ex vivo. To get the properties related to the zero stress sate, the arteries are cut open along their longitudinal axes. We use semi-automatic and automatic techniques to measure parameters related to the waviness and fiber orientation. We show that the straightness parameter (i.e. the ratio between the distances of endpoints of a fiber to the fiber length) is distributed with a beta distribution. The shape of the probability density distribution does not depend on the mean angle orientation of fibers. In addition, our measurements reveal four axially symmetric families of fibers with mean orientations of 0°, 90°, 43° and -43° and circular standard deviations of 40°, 47°, 37° and 37°, with respect to the axial direction, respectively. To the best of our knowledge, this is the first study focusing on structural properties of collagen in the zero stress state and quantifying fiber waviness. The results of this study can be used to develop more precise structural models of the adventitia including waviness and orientational dispersion of fibers. The conclusion section summarizes the main results of the thesis, presents the improvements made over previous studies, and proposes future perspectives of this work.

EPFL2010

Arterial in vitro remodeling

Gabriela Montorzi Thorell

EPFL2004

EPFL2010