Turbulent Stresses in the Region of Aortic and Pulmonary Valves

1982 ◽  
Vol 104 (3) ◽  
pp. 238-244 ◽  
Author(s):  
P. D. Stein ◽  
F. J. Walburn ◽  
H. N. Sabbah

The specific features of turbulent flow that are likely to be damaging to the blood cells and platelets are the stresses which are intrinsic to turbulence, known as Reynolds stresses. These include normal stresses as well as shear stresses. The purpose of this study is to determine the magnitude of the turbulent stresses that may occur during ejection in the vicinity of normal and diseased aortic valves near normal pulmonary valves. Both Reynolds normal stresses and Reynolds shear stresses were calculated from velocities obtained in vitro with a laser Doppler anemometer in the region of two severely stenotic and regurgitant human aortic valves. Reynolds normal stresses were also calculated from velocities obtained with a hot-film anemometer in 21 patients in the region of normal and diseased aortic valves. In seven of these patients, it was calculated in the region of the normal pulmonary valve. The Reynolds normal stress in patients with combined aortic stenosis and insufficiency was prominently higher than in patients with normal valves. In the former, the Reynolds normal stress during ejection transiently reached 18,000 dynes/cm2. This was in the range of the Reynolds normal stress observed in vitro. The Reynolds shear stress measured in vitro transiently reached 11,900 dynes/cm2 during ejection. Because the Reynolds normal stresses in the presence of the severely stenotic and regurgitant valves were comparable in vitro and in patients, it is likely that the Reynolds shear stress in patients is also comparable to values measured in vitro. These values were well above the stresses which, when sustained, have been shown to have a damaging effect upon blood cells and platelets.

1985 ◽  
Vol 107 (3) ◽  
pp. 200-205 ◽  
Author(s):  
F. J. Walburn ◽  
H. N. Sabbah ◽  
P. D. Stein

The purpose of this study was to measure stresses associated with turbulence (Reynolds stresses), in the region of a 29-mm-dia porcine bioprosthetic valve (Hancock, Model 242). Studies were performed in an in vitro pulse duplicating system with the valve mounted in the aortic position. The Reynolds stresses were calculated from velocities obtained with a two channel laser Doppler anemometer. The largest Reynolds shear stress and normal stress occurred at the highest stroke volume used (80 mL). Averaged over ejection they were 38 dynes/cm2 and 380 dynes/cm2, respectively. The maximal instantaneous Reynolds shear stress was 2500 dynes/cm2 and the maximal instantaneous Reynolds normal stress was 6800 dynes/cm2. Stresses of these magnitudes are in the range reported to damage platelets.


Author(s):  
Yertay Mendygarin ◽  
Luis R. Rojas-Solórzano ◽  
Nurassyl Kussaiyn ◽  
Rakhim Supiyev ◽  
Mansur Zhussupbekov

Cardiovascular Diseases, the common name for various Heart Diseases, are responsible for nearly 17.3 million deaths annually and remain the leading global cause of death in the world. It is estimated that this number will grow to more than 23.6 million by 2030, with almost 80% of all cases taking place in low and middle income countries. Surgical treatment of these diseases involves the use of blood-wetted devices, whose relatively recent development has given rise to numerous possibilities for design improvements. However, blood can be damaged when flowing through these devices due to the lack of biocompatibility of surrounding walls, thermal and osmotic effects and most prominently, due to the excessive exposure of blood cells to shear stress for prolonged periods of time. This extended exposure may lead to a rupture of membrane of red blood cells, resulting in a release of hemoglobin into the blood plasma, in a process called hemolysis. Moreover, exposure of platelets to high shear stresses can increase the likelihood of thrombosis. Therefore, regions of high shear stress and residence time of blood cells must be considered thoroughly during the design of blood-contacting devices. Though laboratory tests are vital for design improvements, in-vitro experiments have proven to be costly, time-intensive and ethically controversial. On the other hand, simulating blood behavior using Computational Fluid Dynamics (CFD) is considered to be an inexpensive and promising tool to help predicting blood damage in complex flows. Nevertheless, current state-of-the-art CFD models of blood flow to predict hemolysis are still far from being fully reliable and accurate for design purposes. Previous work have demonstrated that prediction of hemolysis can be dramatically improved when using a multiphase (i.e., phases are plasma, red blood cells and platelets) model of the blood instead of assuming the blood as a homogeneous mixture. Nonetheless, the accurate determination of how the cells segregate becomes the critical issue in reaching a truthful prediction of blood damage. Therefore, the attempt of this study is to develop and validate a numerical model based on Granular Kinetic Theory (GKT) for solid phases (i.e., cells treated as particles) that provides an improved prediction of blood cells segregation within the flow in a microtube. Simulations were based on finite volume method using Eulerian-Eulerian modeling for treatment of three-phase (liquid-red blood cells and platelets) flow including the GKT to deal with viscous properties of the solid phases. GKT proved to be a good model to predict particle concentration and pressure drop by taking into account the contribution of collisional, kinetic and frictional effects in the stress tensor of the segregated solid phases. Preliminary results show that the improved segregated model leads to a better prediction of spatial distribution of blood cells. Simulations were performed using ANSYS FLUENT platform.


2018 ◽  
Vol 41 (11) ◽  
pp. 738-751 ◽  
Author(s):  
Dominica PY Khoo ◽  
Andrew N Cookson ◽  
Harinderjit S Gill ◽  
Katharine H Fraser

Despite the evolution of ventricular assist devices, ventricular assist device patients still suffer from complications due to the damage to blood by fluid dynamic stress. Since rotary ventricular assist devices are assumed to exert mainly shear stress, studies of blood damage are based on shear flow experiments. However, measurements and simulations of cell and protein deformation show normal and shear stresses deform, and potentially damage, cells and proteins differently. The aim was to use computational fluid dynamics to assess the prevalence of normal stress, in comparison with shear stress, in rotary ventricular assist devices. Our calculations showed normal stresses do occur in rotary ventricular assist devices: the fluid volumes experiencing normal stress above 10 Pa were 0.011 mL (0.092%) and 0.027 mL (0.39%) for the HeartWare HVAD and HeartMate II (HMII), and normal stresses over 100 Pa were present. However, the shear stress volumes were up to two orders of magnitude larger than the normal stress volumes. Considering thresholds for red blood cell and von Willebrand factor deformation by normal and shear stresses, the fluid volumes causing deformation by normal stress were between 2.5 and 5 times the size of those causing deformation by shear stress. The exposure times to the individual normal stress deformation regions were around 1 ms. The results clearly show, for the first time, that while blood within rotary ventricular assist devices experiences more shear stress at much higher magnitudes as compared with normal stress, there is sufficient normal stress exposure present to cause deformation of, and potentially damage to, the blood components. This study is the first to quantify the fluid stress components in real blood contacting devices.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
H Yang ◽  
Y Song ◽  
Z Huang ◽  
J Qian ◽  
Z Pang ◽  
...  

Abstract Background Aortic valve disease is the most common valvular heart disease leading to valve replacement. The efficacy of pharmacological therapy for aortic valve disease is limited by the high mechanical stress at the aortic valves impairing the binding rate. We aimed to identify nanoparticle coating with entire platelet membranes to fully mimic their inherent multiple adhesion mechanisms and target the sclerotic aortic valve of apolipoprotein E-deficient (ApoE−/−) mice based on their multiple sites binding capacity under high shear stress. Methods Considering the potent interaction of platelet membrane glycoproteins with components present in sclerotic aortic valves, platelet membrane-coated nanoparticles (PNPs) were synthetized and the binding capacity under high shear stress was evaluated in vitro and in vivo. Results Compared with PNPs bound intensity in the static station, 161%, 59%, and 39% of attached PNPs remained adherent on VWF-, collagen-, and fibrin-coated surfaces under shear stress of 25dyn/cm2 respectively. PNPs demonstrated effectively adhering to von Willebrand factor, collagen and fibrin under shear stresses in vitro. In an aortic valve disease model established in ApoE−/− mice, PNPs group exhibited significant increase of accumulation in the aortic valves compared with PBS and control NP group. PNPs displayed high degrees of proximity or co-localization with vWF, collagen and fibrin, which exhibited good targeting to sclerotic aortic valves by mimicking platelet multiple adhesive mechanisms. Conclusion PNPs could provide a promising platform for the molecular diagnosis and targeting treatment of aortic valve disease. Targeting combination Funding Acknowledgement Type of funding source: Foundation. Main funding source(s): National Natural Science Foundation of China


Lab on a Chip ◽  
2021 ◽  
Author(s):  
YUHAO QIANG ◽  
Jia Liu ◽  
Ming Dao ◽  
E Du

Red blood cells (RBCs) are subjected to recurrent changes in shear stress and oxygen tension during blood circulation. The cyclic shear stress has been identified as an important factor that...


2015 ◽  
Vol 137 (5) ◽  
Author(s):  
Jason Lee ◽  
Aaron B. Baker

In vitro systems for applying mechanical strain to cultured cells are commonly used to investigate cellular mechanotransduction pathways in a variety of cell types. These systems often apply mechanical forces to a flexible membrane on which cells are cultured. A consequence of the motion of the membrane in these systems is the generation of flow and the unintended application of shear stress to the cells. We recently described a flexible system for applying mechanical strain to cultured cells, which uses a linear motor to drive a piston array to create biaxial strain within multiwell culture plates. To better understand the fluidic stresses generated by this system and other systems of this type, we created a computational fluid dynamics model to simulate the flow during the mechanical loading cycle. Alterations in the frequency or maximal strain magnitude led to a linear increase in the average fluid velocity within the well and a nonlinear increase in the shear stress at the culture surface over the ranges tested (0.5–2.0 Hz and 1–10% maximal strain). For all cases, the applied shear stresses were relatively low and on the order of millipascal with a dynamic waveform having a primary and secondary peak in the shear stress over a single mechanical strain cycle. These findings should be considered when interpreting experimental results using these devices, particularly in the case when the cell type used is sensitive to low magnitude, oscillatory shear stresses.


Author(s):  
Adrian P. Sutton

The concept of stress is introduced in terms of interatomic forces acting through a plane, and in the Cauchy sense of a force per unit area on a plane in a continuum. Normal stresses and shear stresses are defined. Invariants of the stress tensor are derived and the von Mises shear stress is expressed in terms of them. The conditions for mechanical equilibrium in a continuum are derived, one of which leads to the stress tensor being symmetric. Stress is also shown to be the functional derivative of the elastic energy with respect to strain,which enables the stress tensor to be derived in models of interatomic forces. Adiabatic and isothermal stresses are distinguished thermodynamically and anharmonicity of atomic interactions is identified as the reason for their differences. Problems set 2 containsfour problems, one of which is based on Noll’s insightful analysis of stress and mechanical equilibrium.


1981 ◽  
Author(s):  
M A Gimbrone ◽  
C F Dewey ◽  
P F Davies ◽  
S R Bussolari

The vascular endothelial lining in vivo is constantly subjected to hemodynamic shear stresses resulting from normal and altered patterns of blood flow. To facilitate the study of effects of fluid shear stress on endothelial cell structure and function, we have developed an in vitro system, utilizing a cone-plate apparatus, to subject coverslip cultures of bovine aortic endothelial cells (BAEC) to controlled levels of shear (up to 102 dynes/cm2) in either laminar or turbulent flow. The magnitude and direction of shear stress within the system are accurately known from both theory and experimental measurements. The data reported here are for laminar flow. Subconfluent BAEC cultures continuously exposed to 1-5 dynes/cm2 shear proliferated at a rate comparable to that of static cultures, and postconfluent monolayers appeared unaltered morphologically for up to 1 week. In contrast, BAEC cultures (both postconfluent and subconfluent) exposed to 8 dynes/cm2 developed dramatic, time-dependent morphological changes. By 48 hrs, cells uniformly assumed an ellipsoidal configuration, with their major axes aligned in the direction of flow. Exposure to >10 dynes/cm2 caused variable cell detachment from plain glass substrates. Cellular migration into linear “wounds”, created in confluent areas, was influenced by both the direction and amplitude of applied shear. Exposure to 8 dynes/ cm2 induced functional alterations, including increased fluid (bulk phase) endocytosis, prostaglandin production and platelet reactivity. These observations indicate that fluid mechanical forces can directly influence endothelial cell structure and function. Hemodynamic modulation of endothelial cell behavior may be relevant to normal vessel wall physiology, as well as the pathogenesis of atherosclerosis and thrombosis.


1990 ◽  
Vol 23 (12) ◽  
pp. 1231-1238 ◽  
Author(s):  
H Nygaard ◽  
M Giersiepen ◽  
J.M Hasenkam ◽  
D Westphal ◽  
P.K Paulsen ◽  
...  

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