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Abstrakty
Aggregation of red blood cells in the micro vasculature may affect blood viscosity in the vessel. The purpose of this study was to investigate the potential effect of non-uniform viscosity caused by red blood cell (RBC) aggregation on nitric oxide (NO) concentration and distribution. A 3-D multi-physics model was established to simulate the production, transport and consumption of NO. Two non-uniform viscosity models caused by RBC aggregation were investigated: one assuming a linear and the other a step hematocrit distribution. In addition, the effect of the thickness of the plasma layer was tested. Simulation results demonstrate that non-uniform viscosity caused by RBCs aggregation influences NO concen-tration distribution. Compared with the uniform viscosity model, NO concentration using non-uniform viscosity is lower than that using uniform viscosity. Moreover, NO concentration calculated from the step hematocrit model is higher than that calculated from the linear hematocrit model. NO concentrations in the endothelium and the vascular wall decrease with the decline of the thickness of the plasma layer. The relative decrease differs between the linear and the step model. Our results suggest that non-uniform viscosity caused by red blood cell aggregation affects nitric oxide distribution in the micro vasculature. If uniform viscosity is assumed when performing numerical simulations, NO concentration values may be overestimated.
Wydawca
Czasopismo
Rocznik
Tom
Strony
341--346
Opis fizyczny
Bibliogr. 21 poz., rys., tab., wykr.
Twórcy
autor
- Key Laboratory for Biomechanics and Mechanobiology of Ministry of Education, School of Biological Science and Medical Engineering, Beihang University, Beijing 100191, China
autor
- Key Laboratory for Biomechanics and Mechanobiology of Ministry of Education, School of Biological Science and Medical Engineering, Beihang University, Beijing 100191, China
autor
- School of Biomedical Engineering, Science and Health Systems, Drexel University, United States
Bibliografia
- [1] Buerk DG, Ances BM, Greenberg JH, Detre JA. Temporal dynamics of brain tissue nitric oxide during functional forepaw stimulation in rats. NeuroImage 2003;18:1–9.
- [2] Ormerod JO, Ashrafian H, Maher AR, Arif S, Steeples V, Born GV, et al. The role of vascular myoglobin in nitrite-mediated blood vessel relaxation. Cardiovasc Res 2011;89:560–5.
- [3] Zhao Y, Brandish PE, Ballou DP, Marletta MA. A molecular basis for nitric oxide sensing by soluble guanylate cyclase. Proc Natl Acad Sci 1999;96:14753–8.
- [4] Bellamy TC, Wood J, Garthwaite J. On the activation of soluble guanylyl cyclase by nitric oxide. Proc Natl Acad Sci 2002;99:507–10.
- [5] Kavdia M, Popel AS. Wall shear stress differentially affects NO level in arterioles for volume expanders and Hb-based O2 carriers. Microvasc Res 2003;66:49–58.
- [6] Chen X, Jaron D, Barbee KA, Buerk DG. The influence of radial RBC distribution, blood velocity profiles, and glycocalyx on coupled NO/O2 transport. J Appl Physiol 2006;100:482–92.
- [7] Chebbi R. Dynamics of blood flow: modeling of the Fåhræus–Lindqvist effect. J Biol Phys 2015;41:313–26.
- [8] Zhang J, Johnson PC, Popel AS. Effects of erythrocyte deformability and aggregation on the cell free layer and apparent viscosity of microscopic blood flows. Microvasc Res 2009;77:265–72.
- [9] Pries AR, Secomb TW, Gessner T, Sperandio MB, Gross JF, Gaehtgens P. Resistance to blood flow in microvessels in vivo. Circ Res 1994;75:904–15.
- [10] Chen X, Buerk D, Barbee K, Kirby P, Jaron D. 3D network model of NO transport in tissue. Med Biol Eng Comput 2011;49:633–47.
- [11] Buerk DG, Barbee KA, Jaron D. Nitric oxide signaling in the microcirculation. Crit Rev Biomed Eng 2011;39:397–433.
- [12] Medvedev AE, Fomin VM. Two-phase blood-flow model in large and small vessels. Dokl Phys 2011;56:610–3.
- [13] Vidya K, Neeraja, Dinesh PA. A mathematical model of two layered magnetic fluid through a catheterized artery. National Conference on Challenges in Research & Technology in the Coming Decades. 2013. pp. 1–5.
- [14] Srivastava VP. Two-phase model of blood flow through stenosed tubes in the presence of a peripheral layer: applications. J Biomech 1996;29:1377–82.
- [15] Sankar DS, Lee U. Two-phase non-linear model for the flow through stenosed blood vessels. J Mech Sci Technol 2007;21:678–89.
- [16] Buerk DG. Can we model nitric oxide biotransport? A survey of mathematical models for a simple diatomic molecule with surprisingly complex biological activities. Annu Rev Biomed Eng 2001;3:109–43.
- [17] Long DS, Smith ML, Pries AR, Klaus L, Damiano ER. Microviscometry reveals reduced blood viscosity and altered shear rate and shear stress profiles in microvessels after hemodilution. Proc Natl Acad Sci U S A 2004;101:10060–5.
- [18] Boodoo C, Bhatt B, Comissiong D. Two-phase fluid flow in a porous tube: a model for blood flow in capillaries. Rheol Acta 2013;52:579–88.
- [19] Chen X, Buerk D, Barbee K, Jaron D. A model of NO/O2 transport in capillary-perfused tissue containing an arteriole and venule pair. Ann Biomed Eng 2007;35:517–29.
- [20] Liu X, Wang Z, Zhao P, Fan Z, Sun A, Zhan F, et al. Nitric oxide transport in normal human thoracic aorta: effects of hemodynamics and nitric oxide scavengers. PLOS ONE 2014;9:e112395.
- [21] Vukosavljevic N, Jaron D, Barbee KA, Buerk DG. Quantifying the L-arginine paradox in vivo. Microvasc Res 2006;71:48–54.
Uwagi
PL
Opracowanie ze środków MNiSW w ramach umowy 812/P-DUN/2016 na działalność upowszechniającą naukę (zadania 2017).
Typ dokumentu
Bibliografia
Identyfikator YADDA
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