动脉狭窄内低密度脂蛋白传输的数值研究：LDL的浓度极化现象

用计算机数值模拟的方法 ,对低密度脂蛋白 ( LDL)在动脉狭窄血管段内的质量传输进行了研究。计算结果表明 ,由于血管壁渗流的存在 ,LDL这样的脂质大分子会聚积在血管的内壁表面 ,发生一种工程上称为浓度极化的现象。LDL浓度在动脉狭窄口后的流动分离点出现峰值。该浓度峰值随雷诺数和动脉狭窄度的增加而呈逐渐下降的趋势。作者认为 ,该区域 LDL浓度的局部升高是引发动脉粥样硬化局部性和动脉狭窄产生的一个非常重要的原因。     

动脉局部狭窄时脉动流的有限元分析

本文利用有限元方法研究动脉局部狭窄下的脉动流流场,重点考查在50％与80％面积狭窄下的速度分布、压力分布、壁面剪应力分布及流动分离情况。几何形状及边界条件均模拟相应的脉动流实验模型。采用测得的随时间变化的速度分布作为入口端条件,并利用罚函数和逆风格式等计算技巧得出了光滑的与实验基本相符的速度、压力波形。本文讨论了不同狭窄下速度、压力、壁面剪应力的分布形态,给出了脉动流中狭窄处局部流动分离的间歇性变化规律,并结合实验与临床应用进行了讨论。     

动脉狭窄对血液流速的影响

为了定量计算动脉局部狭窄对动脉管中血液流动速度的影响，本文分别对狭窄区域内定常流和非定常流动进行了求解，得出了狭窄区域内定常流和脉动流的速度表达式。本文将均匀段的流速形经Ｆｏｕｒｉｅｒ分解成定常和脉动两部分，然后分别计算出狭窄区域内对应的定常和脉动流速，经Ｆｏｕｒｉｅｒ合成还原成流速时域波形，同时针对各种情况将不同狭窄对不同的流速波形的作了分析比较。     

具有缓变狭窄直圆管内的脉动流——早期动脉粥样硬化区的血流动力学机制讨论

六十年代末期以来D.F.Young等人提出了各种数学力学模型对动脉狭窄区血液流动进行理论分析,寻求血流动力学诸因素的定量关系,力图为动脉粥样硬化的发展提供力学上的解释根据。动脉粥样硬化易发区通常在主动脉的较大分枝处及脑动脉和冠状动脉内,血流是脉动的,Reynolds数是O(1)或以上的量级。但D.F.Young等人的研究多数考虑定常流或小Reynolds数的流动,所得结果对动脉粥样硬化狭窄区的血流并不适合。本文考虑Reynolds数为O(1)的量级的冠状动脉狭窄区的脉动流,初步探讨早期动脉粥样硬化狭窄区的血流动力学机制。     

弯曲动脉的血流动力学数值分析

利用计算流体力学的理论和方法对弯曲动脉中的血流动力学进行数值分析，是研究心血管疾病流体动力学机理的一种行之有效的方法。本文将升主动脉、主动脉弓和降主动脉联系起来作为弯曲动脉几何模型，给出了血液流动的边界条件以及计算条件。根据生理脉动流条件，对狗的弯曲动脉几何模型内发展中的血液流动进行了有限元数值模拟，并利用可视化方法对血液流动的轴向速度、二次流、壁面切应力等计算结果进行了分析。研究结果表明，在弯管内侧壁处，同时存在主流方向和二次流方向的回流，此处容易形成涡流。弯管内侧壁比外侧壁的壁面切应力具有更强的脉动性。     

定常流下动脉狭窄局部流场的有限元分析

本文利用有限元数值模拟对定常流下动脉狭窄的局部流场进行了系统研究。在数值模拟中求解非线性轴对称Navier-Stokes方程,并对不同狭窄率、不同雷诺数、不同狭窄形状下的流场速度分布、压力降分布和壁面剪应力分布进行了全面细致的分析和讨论。     

血流动力学数值模拟与动脉粥样硬化研究进展

血流动力学因素被认为与动脉粥样硬化等病理改变密切相关。目前血流动力学数值模拟的对象,主要集中于分支动脉、弯曲动脉以及因血管内膜增生而导致的局部狭窄动脉,这些都是动脉粥样硬化多发的病灶部位。精确的血流动力学数值模拟,必须依赖于解剖精确的血管几何模型和生理真实的血流与管壁有限变形的非线性瞬态流－固耦合。只有在“虚拟血液流动”的基础上,综合考虑血管内的壁面剪应力、粒子滞留时间和氧气的跨血管壁传输等多种因素,血流动力学的数值模拟才能真正有助于人们理解动脉粥样硬化的血流动力学机理,才有可能应用于有关动脉疾病的外科手术规划中。      

明渠中跌坎后突扩分离流数值研究

利用大涡模拟技术，对明渠中跌坎后的二维突扩分离流结构进行了数值模拟，探讨了这类典型分离流各特征区的流动性质，分析了再附区壁面上不同测点处脉动压力的统计特征，并与试验结果进行了比较．在数值模拟中，采用了弱压缩流的控制方程和非均匀网格系统．     

明渠流动若干特性初探

解析定量计算了光滑边壁条件下明渠内部平均流和脉动流能量间的分配关系,得到了平均流粘性耗散能量、脉动流能量、脉动流取自平均流能量之间的关系表达式.分析了能谱的结构形式,从工程应用的角度初步勾勒了恒定流动光滑边壁条件下明渠内部能量分布的轮廓.讨论了壁面剪切流层内的流场结构和特性,研究了Navier-Stokes方程的标度变换等一些定量的指标,从标度和流速分布之间的相互关系入手,对这些指标及其间的相互关系进行了讨论.分析了二维平行壁面剪切流内部流动结构的机理和特性,指出能量传递和不同阶段的不同结构有关,能量耗散和扩散与共振和锁频密切相联系.从另一个角度阐释雷诺数的物理意义,以突出雷诺数和涡之间的关系,强调雷诺数是空间点和时间的函数.     

半浮区液桥热毛细振荡流

采用非定常、三维直接数值模拟方法研究大Pr数半浮区液桥热毛细对流从定常流向振荡流的过渡过程．文中详细描述了热毛细振荡流的起振和振荡特征,给出了液桥横截面上振荡流的流场和温度分布．在地面引力场条件下计算的结果与地面实验的结果进行比较,得出液桥水平截面上的流场和温度分布图样以一定的速度旋转,自由表面固定点处流体的环向流速正、负交替变化的一致结论．     

Effects of fluid recirculation on mass transfer from the arterial surface to flowing blood

The effect of disturbed flow on the mass transfer from arterial surface to flowing blood was studied numerically,and the results were compared with that of our previous work.The arterial wall was assumed to be viscoelastic and the blood was assumed to be incompressible and non-Newtonian fluid,which is more close to human arterial system.Numerical results indicated that the mass transfer from the arterial surface to flowing blood in regions of disturbed flow is positively related with the wall shear rates and it is significantly enhanced in regions of disturbed flow with a local minimum around the reattachment point which is higher than the average value of the downstream.Therefore,it may be implied that the accumulation of cholesterol or lipids within atheromatous plaques is not caused by the reduced efflux of cholesterol or lipids,but by the infiltration of the LDL(low-density lipoprotein) from the flowing blood to the arterial wall.     

Oxygen transfer in human carotid artery bifurcation

Arterial bifurcations are places where blood flow may be disturbed and slow recirculation flow may occur. To reveal the correlation between local oxygen transfer and atherogenesis, a finite element method was employed to simulate the blood flow and the oxygen transfer in the human carotid artery bifurcation. Under steady-state flow conditions, the numerical simulation demonstrated a variation in local oxygen transfer at the bifurcation, showing that the convective condition in the disturbed flow region may produce uneven local oxygen transfer at the blood/wall interface. The disturbed blood flow with formation of slow eddies in the carotid sinus resulted in a depression in oxygen supply to the arterial wall at the entry of the sinus, which in turn may lead to an atherogenic response of the arterial wall, and contribute to the development of atherosclerotic stenosis there. The project supported by the National Natural Science Research Council of China (10632010, 10572017, 30670517).     

The steady/pulsatile flow and macromolecular transport in T-bifurcation blood vessels

IntroductionThefluiddynamicsofbloodcyclesystemplayanimportantroleinthepathogenesisofatherosclerosis.ThephysiologicalanatomyfoundthattheatherosclerosisappearsoftenatthebifurcationorcurvedflowareatoallkindsofRefs.[1 ,2 ] .Theshearstressvariesgreatlyinthoseareaandinfluencesthemacromoleculartransportacrossthebloodwall[3,4].Thus ,theinvestigationoftheflowandmacromoleculartransportinthesecomplexbloodvesselaandthecorrelationbetweenthemareinterestingtoresearchers.Intheseaspect,Liepschstudiedtheflowi…     

BLOOD FLOW AND MACROMOLECULAR TRANSPORT IN CURVED BLOOD VESSELS

A numerical analysis of the steady/pulsatile flow and macromolecular (such as LDL and Albumin) transport in curved blood vessels was carried out. The computational results predict that the vortex of the secondary flow is time-dependent in the aortic arch. The concentration of macromolecule concentrates at the region of sharp curve, and the wall concentration at the outer part is higher than that at the inner part. Atherosclerosis and thrombosis are prone to develop in such regions with sharp flow.     

Computer Simulation of Non-Newtonian Flow and Mass Transport Through Coronary Arterial Stenosis

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Numerical simulation of mass transfer to micropolar fluid flow past a stenosed artery

A mathematical model of unsteady non‐Newtonian blood flow together with the mass transfer through constricted arteries has been developed. The mass transport refers to the movement of atherogenic molecules, i.e. blood‐borne components, such as low‐density lipoproteins from flowing blood into the arterial walls or vice versa. The flowing blood is represented as the suspension of all erythrocytes assumed to be Eringen's micropolar fluid and the arterial wall is considered to be rigid having cosine‐shaped stenosis in its lumen. The mass transfer to blood is controlled by the convection–diffusion equation. The governing equations of motion accompanied by the appropriate choice of the boundary conditions are solved numerically by Marker and Cell method and the results obtained are checked for numerical stability with the desired degree of accuracy. The quantitative analysis carried out finally includes the respective profiles of the flow‐field and the mass concentration along with their distributions over the entire arterial segment as well. The key factors, such as the wall shear stress and Sherwood number, are also examined for further quantitative insight into the flow and the mass transport phenomena through arterial stenosis. The present results show consistency with several existing results in the literature which substantiate sufficiently to validate the applicability of the model under consideration. Copyright © 2010 John Wiley & Sons, Ltd.     

Numerical modelling of shear-dependent mass transfer in large arteries

A numerical scheme for the simulation of blood flow and transport processes in large arteries is presented. Blood flow is described by the unsteady 3D incompressible Navier–Stokes equations for Newtonian fluids; solute transport is modelled by the advection–diffusion equation. The resistance of the arterial wall to transmural transport is described by a shear-dependent wall permeability model. The finite element formulation of the Navier–Stokes equations is based on an operator-splitting method and implicit time discretization. The streamline upwind/Petrov–Galerkin (SUPG) method is applied for stabilization of the advective terms in the transport equation and in the flow equations. A numerical simulation is carried out for pulsatile mass transport in a 3D arterial bend to demonstrate the influence of arterial flow patterns on wall permeability characteristics and transmural mass transfer. The main result is a substantial wall flux reduction at the inner side of the curved region. © 1997 John Wiley & Sons, Ltd.     

An analysis model of pulsatile blood flow in arteries

IntroductionTheperiodicallypulsatilebloodflowinthearterycausesthecircumferentialandaxialmotionoftheelasticbloodvesselandinturntheoscillationofthevesselaffectsthatofthebloodflow .Womersley[1]resolvedsuccessfullythisfluid_solidcouplingproblembysolvingbothlinearNavier_Stokesequationsandthemotionequationsofthethin_walledelastictubeandgainedtheexpressionsofthebloodflowvelocitiesandthevasculardisplacements.Histheoryhasbeenthebasisforthequantitativeanalysisoftherelationshipofthearterialstructureandi…     

Dynamic scaling of unsteady shear-thinning non-Newtonian fluid flows in a large-scale model of a distal anastomosis

Dimensional analysis has been applied to an unsteady pulsatile flow of a shear-thinning power-law non-Newtonian liquid. An experiment was then designed in which both Newtonian and non-Newtonian liquids were used to model blood flow through a large-scale (38.5 mm dia.), simplified, rigid arterial junction (a distal anastomosis of a femorodistal bypass). The flow field within the junction was obtained by Particle Imaging Velocimetry and near-wall velocities were used to calculate the wall shear stresses. Dimensionless wall shear stresses were obtained at different points in the cardiac cycle for two different but dynamically similar non-Newtonian fluids; the good agreement between the measured dimensionless wall shear stresses confirm the validity of the dimensional analysis. However, blood exhibits a constant viscosity at high-shear rates and to obtain complete dynamic similarity between large-scale experiments and life-scale flows, the high-shear viscosity also needs to be included in the analysis. How this might be done is discussed in the paper.