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Hemodynamic assessment of pulmonary hypertension in mice: a model-based analysis of the disease mechanism.
Qureshi, M Umar; Colebank, Mitchel J; Paun, L Mihaela; Ellwein Fix, Laura; Chesler, Naomi; Haider, Mansoor A; Hill, Nicholas A; Husmeier, Dirk; Olufsen, Mette S.
Afiliación
  • Qureshi MU; Department of Mathematics, North Carolina State University, Raleigh, NC, 27695, USA.
  • Colebank MJ; Department of Mathematics, North Carolina State University, Raleigh, NC, 27695, USA.
  • Paun LM; School of Mathematics and Statistics, University of Glasgow, Glasgow, G12 8QQ, UK.
  • Ellwein Fix L; Department of Mathematics and Applied Mathematics, Virginia Commonwealth University, Richmond, VA, 23284, USA.
  • Chesler N; Department of Biomedical Engineering, University of Wisconsin-Madison, Madison, WI, 53706, USA.
  • Haider MA; Department of Mathematics, North Carolina State University, Raleigh, NC, 27695, USA.
  • Hill NA; School of Mathematics and Statistics, University of Glasgow, Glasgow, G12 8QQ, UK.
  • Husmeier D; School of Mathematics and Statistics, University of Glasgow, Glasgow, G12 8QQ, UK.
  • Olufsen MS; Department of Mathematics, North Carolina State University, Raleigh, NC, 27695, USA. msolufse@ncsu.edu.
Biomech Model Mechanobiol ; 18(1): 219-243, 2019 Feb.
Article en En | MEDLINE | ID: mdl-30284059
This study uses a one-dimensional fluid dynamics arterial network model to infer changes in hemodynamic quantities associated with pulmonary hypertension in mice. Data for this study include blood flow and pressure measurements from the main pulmonary artery for 7 control mice with normal pulmonary function and 5 mice with hypoxia-induced pulmonary hypertension. Arterial dimensions for a 21-vessel network are extracted from micro-CT images of lungs from a representative control and hypertensive mouse. Each vessel is represented by its length and radius. Fluid dynamic computations are done assuming that the flow is Newtonian, viscous, laminar, and has no swirl. The system of equations is closed by a constitutive equation relating pressure and area, using a linear model derived from stress-strain deformation in the circumferential direction assuming that the arterial walls are thin, and also an empirical nonlinear model. For each dataset, an inflow waveform is extracted from the data, and nominal parameters specifying the outflow boundary conditions are computed from mean values and characteristic timescales extracted from the data. The model is calibrated for each mouse by estimating parameters that minimize the least squares error between measured and computed waveforms. Optimized parameters are compared across the control and the hypertensive groups to characterize vascular remodeling with disease. Results show that pulmonary hypertension is associated with stiffer and less compliant proximal and distal vasculature with augmented wave reflections, and that elastic nonlinearities are insignificant in the hypertensive animal.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Hemodinámica / Hipertensión Pulmonar / Modelos Biológicos Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Biomech Model Mechanobiol Asunto de la revista: ENGENHARIA BIOMEDICA Año: 2019 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Alemania
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Hemodinámica / Hipertensión Pulmonar / Modelos Biológicos Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: Biomech Model Mechanobiol Asunto de la revista: ENGENHARIA BIOMEDICA Año: 2019 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Alemania