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L A Taber

Publications and source records attributed to L A Taber.

At least 19 recordsLinked to original sources

A 2-D model of flow-induced alterations in the geometry, structure, and properties of carotid arteries.

Evidence from diverse investigations suggests that arterial growth and remodeling correlates well with changes in mechanical stresses from their homeostatic values. Ultimately, therefore, there is a need for a comprehensive theory that accounts for changes in the 3-D distribution of stress within the arterial wall, including residual stress, and its relation to the mechanisms of mechanotransduction. Here, however, we consider a simpler theory that allows competing hypotheses to be tested easily, that can provide guidance in the development of a 3-D theory, and that may be useful in modeling solid-fluid interactions and interpreting clinical data. Specifically, we present a 2-D constrained mixture model for the adaptation of a cylindrical artery in response to a sustained alteration in flow. Using a rule-of-mixtures model for the stress response and first order kinetics for the production and removal of the three primary load-bearing constituents within the wall, we illustrate capabilities of the model by comparing responses given complete versus negligible turnover of elastin. Findings suggest that biological constraints may result in suboptimal adaptations, consistent with reported observations. To build upon this finding, however, there is a need for significantly more data to guide the hypothesis testing as well as the formulation of specific constitutive relations within the model.

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Theoretical and experimental study of growth and remodeling in the developing heart.

A theoretical model is presented for growth and remodeling in the developing embryonic heart. The model is a thick-walled tube composed of two layers of orthotropic pseudoelastic material. The analysis includes stress and strain dependent volumetric growth, with changes in material properties specified to reflect the evolving structure of the heart wall. For use in model validation, experimental measurements of ventricular opening angles are reported for 3-4-day old chick embryos under control and pressure overload conditions. Owing to changes in residual stress in the overloaded heart, the opening angle decreased from 31 +/- 10 degrees to -8 +/- 12 degrees (mean +/- SD) within 12 h and then increased slightly. The opening angle at 12 h was significantly less than the control value. With an appropriate choice of parameters, the model yields reasonable agreement with these and other published opening angle data, as well as with temporal changes in lumen radius, wall thickness, epicardial strains, and pressure-volume curves during development before and after birth.

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Approach to quantify the mechanical behavior of the intact embryonic chick heart.

The heart undergoes remarkable changes during embryonic development due to genetic programing and epigenetic influences such as mechanical loads. An important goal is to develop mathematical models that describe and predict the influence of mechanics on cardiac development, yet the data needed to develop such models remain scant. In particular, prior data from embryonic hearts have come from one-dimensional tests, which reveal well the general characteristic behaviors but are not sufficient for quantifying the complex material behavior exhibited by most soft tissues. We developed a computer-controlled system for quantifying in vitro the multiaxial, regionally dependent mechanical response of the intact embryonic chick heart to controlled distension pressures; such tests have not been accomplished heretofore but promise to contribute to our understanding for they better mimic the native loading conditions and geometry. Calibration of the device indicated that distending the hearts using low flow rates avoids significant viscous losses and thereby allows pressure to be measured directly over small ranges (0-2 mmHg) with good resolution (0.01 mm Hg). Likewise, an on-line video system allows two-dimensional strains to be measured regionally by tracking the motions of triplets of closely spaced (100 microm) microspheres to reasonable resolution (2.5 microm/pixel). Illustrative data from 18 hearts show the utility of the new system, confirm previous findings with regard to the strong viscoelastic response of the stage 18 embryonic chick heart, and provide guidance for the design of future experiments.

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Theoretical model for myocardial trabeculation.

During the morphogenetic process of myocardial trabeculation, most of the cardiac jelly of the initially smooth-walled heart is replaced by sponge-like muscle. The mechanisms that drive and regulate this important process are poorly understood. Using a theoretical model, we examined the possible role that cytoskeletal contraction plays during the initial stages of trabeculation. The myocardium is modeled as a thin viscoelastic membrane consisting of contractile (stress) fibers embedded in an isotropic incompressible matrix, with the interaction of myocardial cells and cardiac jelly fibers providing long-range mechanical effects. The stress fibers are assumed to behave like smooth muscle and to normally operate on the descending limb of their stress-stretch curve. Mechanical instability due to the effectively negative stiffness then leads to the creation of pattern. As a first approximation, computations were carried out for a flat rectangular membrane with stress fibers aligned along a single direction. The computed deformation patterns depend strongly on the magnitude and anisotropy of the long-range effects. Given plausible assumptions about the mechanical properties of the embryonic heart, the model predicts trabecular patterns similar to those observed in the embryo, including the development of circumferential ridges and relatively thin regions ("holes") in the trabecular sheets.

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Investigating Murray's law in the chick embryo.

According to the optimization principle known as Murray's law, the blood vessel geometry at a bifurcation satisfies the relation alpha = (D3(1) + D3(2))/D3(0) = 1, where D0, D1, and D2 are the diameters of the parent and two daughter vessels, respectively. Previous investigations have shown that mature blood vessels adhere to this law fairly closely. The purpose of this study was to test Murray's law in the developing extraembryonic blood vessels of 2-4 day-old chick embryos. Vessel diameters were measured manually using image analysis software. The measurements for the group of all vessels at all studied stages (n = 449) gave alpha = 1.01+/-0.34 (mean +/- SD), and the value of alpha is similar at all stages. These results indicate that Murray's law holds in the chick embryo, even before medial smooth muscle becomes functional, suggesting that blood vessels follow the same basic morphogenetic rules throughout life.

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Stress-modulated growth, residual stress, and vascular heterogeneity.

A simple phenomenological model is used to study interrelations between material properties, growth-induced residual stresses, and opening angles in arteries. The artery is assumed to be a thick-walled tube composed of an orthotropic pseudoelastic material. In addition, the normal mature vessel is assumed to have uniform circumferential wall stress, which is achieved here via a mechanical growth law. Residual stresses are computed for three configurations: the unloaded intact artery, the artery after a single transmural cut, and the inner and outer rings of the artery created by combined radial and circumferential cuts. The results show that the magnitudes of the opening angles depend strongly on the heterogeneity of the material properties of the vessel wall and that multiple radial and circumferential cuts may be needed to relieve all residual stress. In addition, comparing computed opening angles with published experimental data for the bovine carotid artery suggests that the material properties change continuously across the vessel wall and that stress, not strain, correlates well with growth in arteries.

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Biomechanics of cardiovascular development.

It long has been known that mechanical forces play a role in the development of the cardiovascular system, but only recently have biomechanical engineers begun to explore this field. This paper reviews some of this work. First, an overview of the relevant biology is discussed. Next, a mechanical theory is presented that can be used to model developmental processes. The theory includes the effects of finite volumetric growth and active contractile forces. Finally, applications of this and other theories to problems of cardiovascular development are discussed, and some future directions are suggested. The intent is to stimulate further interest among engineers in this important area of research.

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Biomechanical growth laws for muscle tissue.

It is generally accepted that growth of muscle tissue depends in part on biomechanical factors. However, the precise relationships that govern mechanically induced growth are not known. This paper uses available data to propose a set of biomechanical growth laws for striated and smooth muscle. For striated muscle fibers, transverse and longitudinal growth are hypothesized to depend on the active and passive fiber stress, respectively. For smooth muscle fibers in arteries, transverse growth is assumed to depend on the fiber stress (active behavior is ignored), with longitudinal growth depending on both fiber stress and the shear stress on the endothelium due to blood flow. In both types of muscle, the rate of growth is assumed to depend linearly on the stresses. Relatively simple models for skeletal muscle, the heart, and arteries are used to show that the proposed growth laws can predict many of the known characteristics of muscle growth during development and following load perturbations in the mature animal.

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An optimization principle for vascular radius including the effects of smooth muscle tone.

An optimization principle is proposed for the regulation of vascular morphology. This principle, which extends Murray's law, is based on the hypothesis that blood vessel diameter is controlled by a mechanism that minimizes the total energy required to drive the blood flow, to maintain the blood supply, and to support smooth muscle tone. A theoretical analysis reveals that the proposed principle predicts that the optimum shear stress on the vessel wall due to blood flow increases with blood pressure. This result agrees qualitatively with published findings that the fluid shear stress in veins is significantly smaller than it is in arteries.

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Mechanical aspects of cardiac development.

Heart development depends on a dynamic interaction between genetic and epigenetic factors. This paper discusses some of the biomechanical processes that help shape the heart in the embryo. First, an overview is given of some of the critical events that occur during cardiac development. Next, mechanics and modeling strategies are discussed for the morphogenetic processes of cardiac tube formation, cardiac looping, myocardial trabeculation, septation, valve formation, and muscle-fiber alignment. Finally, some considerations for future work in this area are listed.

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A model for aortic growth based on fluid shear and fiber stresses.

Stress-modulated growth in the aorta is studied using a theoretical model. The model is a thick-walled tube composed of two pseudoelastic, orthotropic layers representing the intima/media and the adventitia. Both layers are assumed to follow a growth law in which the time rates of change of the growth stretch ratios depend linearly on the local smooth muscle fiber stress and on the shear stress due to blood flow on the endothelium. Using finite elasticity theory modified to include volumetric growth, we computed temporal changes in stress, geometry, and opening angle (residual strain) during development and following the onset of sudden hypertension. For appropriate values of the coefficients in the growth law, the model yields results in reasonable agreement with published data for global and local growth of the rat aorta.

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Passive stress-strain measurements in the stage-16 and stage-18 embryonic chick heart.

The first stress-strain measurements on embryonic cardiovascular tissue are described here, obtained from cyclic uniaxial loading of the primitive ventricle. An excised ventricular segment from Hamburger/Hamilton stage-16 or stage-18 chicks (2-1/2 and 3 days of a 21-day incubation period) was mounted longitudinally between two small wires in oxygenated Krebs-Henseleit cardioplegia solution. One wire was attached to an ultrasensitive force transducer and the other to a Huxley micromanipulator controlled by remote motor drive. A real-time video tracking system calculated three myocardial surface strains based on the positions of three surface markers while the heart was deformed in a triangular wave pattern. Force transducer output was filtered, digitally sampled, and stored with strains and time. Results were plotted as strain (longitudinal, circumferential, shear, and principal) versus time, stress versus time, and stress versus longitudinal strain. The stress-strain curves were nonlinear, even at low strain levels. The hysteresis loops were large; mean hysteresis energy as a proportion of total cycle stored strain energy was 36 percent (stage 16) and 41 percent (stage 18). We created a finite element model of the ventricle and fit the model behavior to the experimental behavior to determine parameters for a stage-18 pseudoelastic strain-energy function of exponential form. The calculated exponential parameter is significantly lower than that found in corresponding uniaxial studies of mature myocardium, possibly indicating the lower fiber content of the immature tissue. The results of this study are the first step in characterizing material properties for comparisons with later developmental stages and with impaired and altered myocardium. The long-term goal is to aid in identifying the biomechanical factors regulating growth and morphogenesis.

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Theoretical study of stress-modulated growth in the aorta.

A theoretical model is presented for stress-modulated growth in the aorta. The model consists of a pseudoelastic tube composed of two layers representing the intima/media and the adventitia. Finite volumetric growth is included by letting the time-rate of change of the zero-stress dimensions of each volume element depend linearly on the local stresses. After analysing the model, we examine its fundamental growth response under changes in loads, material properties, and growth parameters. The behavior of the model is quite sensitive to changes in material nonlinearity and in the coefficients of the growth law. Next, growth of the aorta is simulated during development and maturity. For an appropriate choice of the parameters, the model exhibits patterns of growth that agree qualitatively with known characteristics of aortic growth. Comparison of model results with published experimental data during hypertension in the rat shows good agreement in the time course of the vessel radii and residual strain. Finally, the implications of the results are discussed in the context of deducing a general mechanical growth law for soft tissues. The proposed model should be useful in studies to determine the biomechanical factor that regulates growth.

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Mechanics of ventricular torsion.

Recent research suggests that left ventricular torsion is an important indicator of cardiac function. We used two theoretical models to study the mechanics of this phenomenon: a compressible cylinder and an incompressible ellipsoid of revolution. The analyses of both models account for large- strain passive and active material behavior, with a muscle fiber angle that varies linearly from endocardium to epicardium. Relative to the end- diastolic configuration, the predicted torsion exhibits several experimentally observed features, including a peak near end systole, rapid untwisting during isovolumic relaxation, and increased twist near the apex. The magnitude of the twist is sensitive to the fiber architecture, the ventricular geometry, and the compressibility and contractility of the myocardium. In particular, the model predicts that the systolic twist increases with increasing compressibility, contractility, and wall thickness, while it decreases with increasing cavity volume. The peak twist approximately doubles (from about 0.02 to 0.04 rad cm(-1)) with a doubling of myocardial compressibility or with a change in the endocardial/epicardial muscle fiber angles from 90/ -90 degrees to 60/ -60 degrees. The twist is less sensitive to changes in contractility and ventricular geometry. These findings provide a basis for interpreting measurements of ventricular torsion in the clinical setting.

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Mechanics of cardiac looping.

During the early stages of embryonic development, the heart is a smooth-walled, muscle-wrapped tube that bends and rotates in a vital, but poorly understood, morphogenetic process called looping. Since looping involves biomechanical forces, this paper examines two mechanically based hypotheses for the bending component of cardiac looping. The first hypothesis is that an initial tension in or near the dorsal mesocardium (DM), a longitudinal structure along the outside of the ventricle, drives the deformation. To relieve the bending stresses in the tube, the myocytes change shape passively, and then they deform actively to continue the process to completion of a full loop. In the second hypothesis, contraction of circumferentially arranged actin macrofilaments produces circumferential compression and longitudinal expansion (due to incompressibility) of the myocytes. The DM locally constrains the longitudinal deformation, forcing the tube to bend. The feasibility of these hypotheses was evaluated using theoretical models and published experimental results. The models, which consist of beams composed of two layers representing the DM and the ventricular myocardium, show that the hypotheses are consistent with most of the known data, but further studies are necessary. In this regard, the models provide a conceptual framework for designing experiments to investigate the mechanics of looping.

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A model for stress-induced growth in the developing heart.

Mechanical loads affect growth and morphogenesis in the developing heart. Using a theoretical model, we studied stress-modulated growth in the embryonic chick ventricle during stages 21-29 (4-6 days of a 21-day incubation period). The model is a thick-walled, compressible, pseudoelastic cylinder, with finite volumetric growth included by letting the rate of change of the local zero-stress configuration depend linearly on the Cauchy stresses. After investigating the fundamental behavior of the model, we used it to study global and local growth in the primitive ventricle due to normal and abnormal cavity pressures. With end-diastolic pressure taken as the growth-modulating stimulus, correlating theoretical and available experimental results yielded the coefficients of the growth law, which was assumed to be independent of time and loading conditions. For both normal and elevated pressures, the predicted changes in radius and wall volume during development were similar to experimental measurements. In addition, the residual stress generated by differential growth agreed with experimental data. These results suggest that wall stress may be a biomechanical factor that regulates growth in the embryonic heart.

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Mechanical effects of looping in the embryonic chick heart.

During early embryonic development, the heart bends into a curved tube in a vital morphogenetic process called looping. Since looping involves poorly understood biomechanical forces that are difficult to measure, this paper presents a theoretical model for the tubular chick heart, whose development is similar to that of the human heart. Representing the basic morphology of the looped ventricle, the model is a thick-walled, isotropic, pressurized curved tube composed of three layers representing the myocardium, cardiac jelly, and endocardium. The model is analyzed with nonlinear elasticity theory, modified to include residual strain and muscle activation, and material properties are determined by correlating theoretical and experimental pressure-volume relations. The results show that longitudinal curvature significantly influences the biomechanical behavior of the embryonic heart. As the curvature increases, the compliance of the tube increases, especially at end systole. Stress concentrations, which develop in the endocardium during diastole and in the myocardium during systole, also increase with the curvature. The largest wall stress during the cardiac cycle occurs near the beginning of systolic ejection in the myocardial layer at the inner curvature of the tube. Relative to end diastole, the model predicts epicardial strains that are nearly equal in the circumferential and meridional directions, in agreement with experimental measurements. These results provide insight into the interrelation between biomechanical forces and morphogenesis during cardiac looping.

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