Biomedical subjects

Peter J Hunter

Publications and source records attributed to Peter J Hunter.

8 recordsLinked to original sources

PubMed2004

Development of an in vivo method for determining material properties of passive myocardium.

Calculation of mechanical stresses and strains in the left ventricular (LV) myocardium by the finite element (FE) method relies on adequate knowledge of the material properties of myocardial tissue. In this paper, we present a model-based estimation procedure to characterize the stress-strain relationship in passive LV myocardium. A 3D FE model of the LV myocardium was used, which included morphological fiber and sheet structure and a nonlinear orthotropic constitutive law with different stiffness in the fiber, sheet, and sheet-normal directions. The estimation method was based on measured wall strains. We analyzed the method's ability to estimate the material parameters by generating a set of synthetic strain data by simulating the LV inflation phase with known material parameters. In this way we were able to verify the correctness of the solution and to analyze the effects of measurement and model error on the solution accuracy and stability. A sensitivity analysis was performed to investigate the observability of the material parameters and to determine which parameters to estimate. The results showed a high degree of coupling between the parameters governing the stiffness in each direction. Thus, only one parameter in each of the three directions was estimated. For the tested magnitudes of added noise and introduced model errors, the resulting estimated stress-strain characteristics in the fiber and sheet directions converged with good accuracy to the known relationship. The sheet-normal stress-strain relationship had a higher degree of uncertainty as more noise was added and model error was introduced.

Algorithms↗

PubMed2004

Modeling RBC and neutrophil distribution through an anatomically based pulmonary capillary network.

An anatomically based finite element model of the human pulmonary microcirculation has been created and applied to simulating regional variations in blood flow. A geometric mesh of the capillary network over the surface of a single alveolar sac is created using a Voronoi meshing technique. A pressure-flow relationship that describes blood cell transit is implemented in the network. Regional flow is investigated by imposing gravity-dependent transpulmonary and transmural boundary conditions. Comparisons of red and white blood cell transit times in the upper, mid, and lower lung showed physiologically consistent trends of a decreasing average transit time and an increased homogeneity of transit time distributions as a result of increasing average capillary diameter and flow down the height of a vertical lung. The model was found to reproduce experimentally consistent trends in red blood cell transit times and relative blood flows with respect to lung height. This model enables flow properties and cell transit time behavior in the pulmonary microcirculation under varying conditions, for example in different "zones" of the lung, to be explored.

Blood Flow Velocity↗

PubMed2004

Modeling water vapor and heat transfer in the normal and the intubated airways.

Intubation of the artificially ventilated patient with an endotracheal tube bypasses the usual conditioning regions of the nose and mouth. In this situation any deficit in heat or moisture in the air is compensated for by evaporation and thermal transfer from the pulmonary airway walls. To study the dynamics of heat and water transport in the intubated airway, a coupled system of nonlinear equations is solved in airway models with symmetric geometry and anatomically based geometry. Radial distribution of heat, water vapor, and velocity in the airway are described by power-law equations. Solution of the time-dependent system of equations yields dynamic airstream and mucosal temperatures and air humidity. Comparison of model results with two independent experimental studies in the normal and intubated airway shows a close correlation over a wide range of minute ventilation. Using the anatomically based model a range of spatially distributed temperature paths is demonstrated, which highlights the model's ability to predict thermal behavior in airway regions currently inaccessible to measurement. Accurate representation of conducting airway geometry is shown to be necessary for simulating mouth-breathing at rates between 15 and 100 l x min(-1), but symmetric geometry is adequate for the low minute ventilation and warm inspired air conditions that are generally supplied to the intubated patient.

Computer Simulation↗

PubMed2003

Integration from proteins to organs: the Physiome Project.

The Physiome Project will provide a framework for modelling the human body, using computational methods that incorporate biochemical, biophysical and anatomical information on cells, tissues and organs. The main project goals are to use computational modelling to analyse integrative biological function and to provide a system for hypothesis testing.

Computer Simulation↗

PubMed2003

One-dimensional rabbit sinoatrial node models: benefits and limitations.

INTRODUCTION: Cardiac multicellular modeling has traditionally focused on ventricular electromechanics. More recently, models of the atria have started to emerge, and there is much interest in addressing sinoatrial node structure and function. METHODS AND RESULTS: We implemented a variety of one-dimensional sinoatrial models consisting of descriptions of central, transitional, and peripheral sinoatrial node cells, as well as rabbit or human atrial cells. These one-dimensional models were implemented using CMISS on an SGI Origin 2000 supercomputer. Intercellular coupling parameters recorded in experimental studies on sinoatrial node and atrial cell-pairs under-represent the electrotonic interactions that any cardiomyocyte would have in a multidimensional setting. Unsurprisingly, cell-to-cell coupling had to be scaled-up (by a factor of 5) in order to obtain a stable leading pacemaker site in the sinoatrial node center. Further critical parameters include the gradual increase in intercellular coupling from sinoatrial node center to periphery, and the presence of electrotonic interaction with atrial cells. Interestingly, the electrotonic effect of the atrium on sinoatrial node periphery is best described as opposing depolarization, rather than necessarily hyperpolarizing, as often assumed. CONCLUSION: Multicellular one-dimensional models of sinoatrial node and atrium can provide useful insight into the origin and spread of normal cardiac excitation. They require larger than "physiologic" intercellular conductivities in order to make up for a lack of "anatomical" spatial scaling. Multicellular models for more in-depth quantitative studies will require more realistic anatomico-physiologic properties.

Action Potentials↗

PubMed2003

Modeling total heart function.

Computational models of the electrical and mechanical function of the heart are reviewed. These models attempt to explain the integrated function of the heart in terms of ventricular anatomy, the structure and material properties of myocardial tissue, the membrane ion channels, and calcium handling and myofilament mechanics of cardiac myocytes. The models have established the computational framework for linking the structure and function of cardiac cells and tissue to the integrated behavior of the intact heart, but many more aspects of physiological function, including metabolic and signal transduction pathways, need to be included before significant progress can be made in understanding many disease processes.

Animals↗

PubMed2002

Cardiac microstructure: implications for electrical propagation and defibrillation in the heart.

Our understanding of the electrophysiological properties of the heart is incomplete. We have investigated two issues that are fundamental to advancing that understanding. First, there has been widespread debate over the mechanisms by which an externally applied shock can influence a sufficient volume of heart tissue to terminate cardiac fibrillation. Second, it has been uncertain whether cardiac tissue should be viewed as an electrically orthotropic structure, or whether its electrical properties are, in fact, isotropic in the plane orthogonal to myofiber direction. In the present study, a computer model that incorporates a detailed three-dimensional representation of cardiac muscular architecture is used to investigate these issues. We describe a bidomain model of electrical propagation solved in a discontinuous domain that accurately represents the microstructure of a transmural block of rat left ventricle. From analysis of the model results, we conclude that (1) the laminar organization of myocytes determines unique electrical properties in three microstructurally defined directions at any point in the ventricular wall of the heart, and (2) interlaminar clefts between layers of cardiomyocytes provide a substrate for bulk activation of the ventricles during defibrillation.

Animals↗

PubMedDate not supplied

Sarcomere length changes in a 3D mathematical model of the pig ventricles.

Measurements of the geometry and fibrous-sheet structure of the left and right ventricles of the pig heart are fitted with a finite element model. Mechanical changes during the heart cycle are computed by solving the equations of motion under specified ventricular boundary conditions and using experimentally defined constitutive laws for the active and passive material properties of myocardial tissue. The resulting patterns of deformation, such as axial torsion and changes in wall thickness and base-apex length, are consistent with experimental observations. The model can therefore be used to predict sarcomere length changes and other strain patterns throughout the myocardium and throughout the cardiac cycle. Here we present sarcomere length changes at a limited number of material points within the wall. Sarcomere length typically varies by 10% above and below the unloaded length; although under the boundary conditions imposed in the current model the midwall circumferentially oriented sarcomere lengths increased by up to 20% at end diastole. We provide web-access details for a downloadable software program designed to provide more extensive information on mechanical deformation, such as the principal strains and muscle fibre cross-sectional area changes during the cardiac cycle.

Animals↗