Effect of Blood Viscosity on Oxygen Transport in Residual Stenosed Artery Following Angioplasty

2008 ◽  
Vol 130 (1) ◽  
Author(s):  
Ohwon Kwon ◽  
Mahesh Krishnamoorthy ◽  
Young I. Cho ◽  
John M. Sankovic ◽  
Rupak K. Banerjee
Keyword(s):  
Flow Rate ◽  
Oxygen Transport ◽  
Blood Viscosity ◽  
Recirculation Zone ◽  
Binding Capacity ◽  
Vasa Vasorum ◽  
Oxygen Binding ◽  
Stenosed Artery ◽  
Hyperemic Flow ◽  
Basal Flow

The effect of blood viscosity on oxygen transport in a stenosed coronary artery during the postangioplasty scenario is studied. In addition to incorporating varying blood viscosity using different hematocrit (Hct) concentrations, oxygen consumption by the avascular wall and its supply from vasa vasorum, nonlinear oxygen binding capacity of the hemoglobin, and basal to hyperemic flow rate changes are included in the calculation of oxygen transport in both the lumen and the avascular wall. The results of this study show that oxygen transport in the postangioplasty residual stenosed artery is affected by non-Newtonian shear-thinning property of the blood viscosity having variable Hct concentration. As Hct increases from 25% to 65%, the diminished recirculation zone for the increased Hct causes the commencement of pO2 decrease to shift radially outward by ∼20% from the center of the artery for the basal flow, but by ∼10% for the hyperemic flow at the end of the diverging section. Oxygen concentration increases from a minimum value at the core of the recirculation zone to over 90mmHg before the lumen-wall interface at the diverging section for the hyperemic flow, which is attributed to increased shear rate and thinner lumen boundary layer for the hyperemic flow, and below 90mmHg for the basal flow. As Hct increases from 25% to 65%, the average of pO2,min beyond the diverging section drops by ∼25% for the basal flow, whereas it increases by ∼15% for the hyperemic flow. Thus, current results with the moderate stenosed artery indicate that reducing Hct might be favorable in terms of increasing O2 flux and pO2,min, in the medial region of the wall for the basal flow, while higher Hct is advantageous for the hyperemic flow beyond the diverging section. The results of this study not only provide significant details of oxygen transport under varying pathophysiologic blood conditions such as unusually high blood viscosity and flow rate, but might also be extended to offer implications for drug therapy related to blood-thinning medication and for blood transfusion and hemorrhage.

Coupled Oxygen Transport in the Avascular Region of a Coronary Artery for Basal to Hyperemic Flow

2004 ◽  
Author(s):  
Vinayak Vaidya ◽  
Lloyd H. Back ◽  
Rupak K. Banerjee
Keyword(s):  
Coronary Artery ◽  
Oxygen Transport ◽  
Binding Capacity ◽  
Vasa Vasorum ◽  
Wall Region ◽  
Flow Rates ◽  
Concentration Boundary ◽  
Factors Affecting ◽  
O2 Concentration ◽  
Hyperemic Flow

The numerical investigation of coupled oxygen transport to the avascular region of the wall of coronary artery is carried out for varying wall thickness and flow rates from basal to hyperemic condition. The factors affecting the O2 transport, such as, consumption of oxygen in the avascular wall region, w, the avascular thickness, δ, supply of O2 from vasa vasorum, nonlinear O2 binding capacity of the hemoglobin and varying flow rates, are taken into account. The O2 concentration boundary layer, δb, is observed to be of ~80 μm thickness. The lowest medial partial pressure, Po2,min decreases by ~80% for a larger avascular thickness, δ, of 300 μm when compared with that for smaller δ of 200 μm.

scholarly journals Energy Loss in Steep Open Channels with Step-Pools

Water ◽  
2020 ◽  
Vol 13 (1) ◽  
pp. 72
Author(s):  
Suresh Kumar Thappeta ◽  
S. Murty Bhallamudi ◽  
Venu Chandra ◽  
Peter Fiener ◽  
Abul Basar M. Baki
Keyword(s):  
Energy Loss ◽  
Flow Rate ◽  
Recirculation Zone ◽  
Three Dimensional ◽  
Nonlinear Function ◽  
Open Channels ◽  
Geometrical Parameters ◽  
Transition Flow ◽  
Cumulative Energy ◽  
Zone Velocity

Three-dimensional numerical simulations were performed for different flow rates and various geometrical parameters of step-pools in steep open channels to gain insight into the occurrence of energy loss and its dependence on the flow structure. For a given channel with step-pools, energy loss varied only marginally with increasing flow rate in the nappe and transition flow regimes, while it increased in the skimming regime. Energy loss is positively correlated with the size of the recirculation zone, velocity in the recirculation zone and the vorticity. For the same flow rate, energy loss increased by 31.6% when the horizontal face inclination increased from 2° to 10°, while it decreased by 58.6% when the vertical face inclination increased from 40° to 70°. In a channel with several step-pools, cumulative energy loss is linearly related to the number of step-pools, for nappe and transition flows. However, it is a nonlinear function for skimming flows.

scholarly journals Quantitative Monitoring of Dynamic Blood Flows Using Coflowing Laminar Streams in a Sensorless Approach

2021 ◽  
Vol 11 (16) ◽  
pp. 7260
Author(s):  
Yang Jun Kang
Keyword(s):  
Blood Flow ◽  
Flow Rate ◽  
Blood Viscosity ◽  
Measurement Errors ◽  
Present Method ◽  
Test Fluid ◽  
Constant Flow Rate ◽  
Rbc Aggregation ◽  
Sinusoidal Flow ◽  
Analytical Expressions

Determination of blood viscosity requires consistent measurement of blood flow rates, which leads to measurement errors and presents several issues when there are continuous changes in hematocrit changes. Instead of blood viscosity, a coflowing channel as a pressure sensor is adopted to quantify the dynamic flow of blood. Information on blood (i.e., hematocrit, flow rate, and viscosity) is not provided in advance. Using a discrete circuit model for the coflowing streams, the analytical expressions for four properties (i.e., pressure, shear stress, and two types of work) are then derived to quantify the flow of the test fluid. The analytical expressions are validated through numerical simulations. To demonstrate the method, the four properties are obtained using the present method by varying the flow patterns (i.e., constant flow rate or sinusoidal flow rate) as well as test fluids (i.e., glycerin solutions and blood). Thereafter, the present method is applied to quantify the dynamic flows of RBC aggregation-enhanced blood with a peristaltic pump, where any information regarding the blood is not specific. The experimental results indicate that the present method can quantify dynamic blood flow consistently, where hematocrit changes continuously over time.

A Meanline Model for Impeller Flow Recirculation

2008 ◽  
Author(s):  
Xuwen Qiu ◽  
David Japikse ◽  
Mark Anderson
Keyword(s):  
Flow Rate ◽  
Recirculation Zone ◽  
Reverse Flow ◽  
Low Flow ◽  
Suction Surface ◽  
Blade Loading ◽  
Flow Recirculation ◽  
Impeller Outlet ◽  
Active Flow ◽  
Low Flow Rate

Flow recirculation at the impeller inlet and outlet is an important feature that affects impeller performance, especially the power consumption at a very low flow rate. Although the mechanisms for this flow phenomenon have been studied, a practical model is needed for meanline modeling of impeller off-design performance. In this paper, a meanline recirculation model is proposed. At the inlet, the recirculation zone acts as area blockage to relieve the large incidence of the active flow at a low flow rate. The size of the blockage is estimated through a critical area ratio of an artificial “inlet diffuser” from the inlet to throat. The intensity of the reverse flow can then be calculated by assuming a linear velocity profile of meridional velocity in the recirculation zone. At the impeller outlet, a recirculation zone near the suction surface is established to balance the velocity difference on the pressure and suction sides of the blade. The size and the intensity of the outlet recirculation zone is assumed related to blade loading, which can be evaluated based on flow turning and Coriolis force. A few validation cases are presented showing a good comparison between test data and prediction by the model.

Physical basis of the dependence of blood viscosity on tube radius

1960 ◽  
Vol 198 (6) ◽  
pp. 1193-1200 ◽  
Author(s):  
Robert H. Haynes
Keyword(s):  
Flow Rate ◽  
Blood Viscosity ◽  
Apparent Viscosity ◽  
Hind Limb ◽  
Marginal Zone ◽  
Tube Wall ◽  
Effective Diameter ◽  
Tube Radius ◽  
Vascular Bed ◽  
A Cell

Two theories are applied to measurements of the decrease in apparent viscosity of blood in narrow tubes (Fahraeus-Lindqvist effect). First, the effect may be attributed to the presence of unsheared laminae in the fluid (sigma phenomenon), and it was found that the thickness of such laminae must vary between 3.5 µ at 10% hematocrit and 34 µ at 80%. Alternatively, the effect may be caused by a cell-free marginal zone adjacent to the tube wall, which would have to be 6 µ thick at 10% hematocrit and 1.5 µ at 80%. There is a slight suggestion in the data that the effect may be reversed as the flow rate approaches zero (i.e. the apparent viscosity rises in small tubes). Finally, a method is proposed for calculating the effective diameter of a vascular bed, and it was found to be 55 µ for a dog's hind limb.

Abstract 192: A Hypothesis on Initiation of Coronary Atherosclerosis: The Role of Intimal Neovascularization and Proliferation. Do Lipoproteins Invade Coronary Tunica Intima from the Opposite Site?

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Vladimir M Subbotin
Keyword(s):  
Coronary Atherosclerosis ◽  
Binding Capacity ◽  
Good Reason ◽  
Single Layer ◽  
Vasa Vasorum ◽  
Great Expectations ◽  
Diffuse Intimal Thickening ◽  
Arterial Intima ◽  
Capillary Bed

Objectives Tremendous success of statins in coronary atherosclerosis (CA) prevention offered great expectations for extended protection and effective therapeutics. However, stalled progress in pharmaceutical treatment gives a good reason to review whether the hypothesis underlining our efforts is consistent with undoubted facts on coronary artery in normal and diseased forms. Analysis An accepted hypothesis states that CA is initiated by endothelial dysfunction due to inflammation and high levels of LDL, followed by lipids and macrophage penetration into arterial intima and plaque formation. It is crucial to highlight that normal coronary intima is not a single-layer endothelium covering thin acellular compartment, as is commonly claimed in most publications, but always appears as a multi-layer cellular compartment, or diffuse intimal thickening (DIT), where cells are arranged in a few dozens layers. Since it is unanimously agreed that LDL invade DIT from lumen, the initial depositions ought to be most proximal to blood, i.e. in inner DIT layers. The facts show that the opposite is true, and lipids are deposited in the outer DIT. This contradiction is resolved by noting that normal DIT is always avascular, receiving oxygen and nutrients by diffusion from lumen, whereas in CA outer DIT is always neovascularized from adventitial vasa vasorum . Proteoglycan biglycan, confined to outer DIT of normal and diseased coronary, has high binding capacity for LDL. However, normal DIT is avascular, whereas in CA biglycan of outer DIT layers appears in direct contact with blood and extract lipoproteins. These facts explain patterns and mechanisms of CA initiation, which is not unique: normally avascular cornea accumulates lipoproteins after neovascularization, resulting in lipid keratopathy. The author offers a hypothesis on neovascularization. Cells in coronary DIT possess high proliferative capacity. Excessive cell replication increases DIT thickness, impairs diffusion, resulting in hypoxia of outer DIT. Hypoxia induces neovascularization of outer DIT layers, where biglycan extracts LDL from newly formed capillary bed, initiating CA. Conclusion Controls of cell proliferation and neovascularization in coronary DIT should be a priority of our research.

scholarly journals The role of oxygen transport in atherosclerosis and vascular disease

2020 ◽  
Vol 17 (165) ◽  
pp. 20190732 ◽  
Author(s):  
John Tarbell ◽  
Marwa Mahmoud ◽  
Andrea Corti ◽  
Luis Cardoso ◽  
Colin Caro
Keyword(s):  
Blood Flow ◽  
Vascular Disease ◽  
Oxygen Transport ◽  
Intimal Hyperplasia ◽  
Hypoxia Inducible Factor ◽  
Vascular Diseases ◽  
Vascular Wall ◽  
Vasa Vasorum ◽  
Mechanical Factors

Atherosclerosis and vascular disease of larger arteries are often associated with hypoxia within the layers of the vascular wall. In this review, we begin with a brief overview of the molecular changes in vascular cells associated with hypoxia and then emphasize the transport mechanisms that bring oxygen to cells within the vascular wall. We focus on fluid mechanical factors that control oxygen transport from lumenal blood flow to the intima and inner media layers of the artery, and solid mechanical factors that influence oxygen transport to the adventitia and outer media via the wall's microvascular system—the vasa vasorum (VV). Many cardiovascular risk factors are associated with VV compression that reduces VV perfusion and oxygenation. Dysfunctional VV neovascularization in response to hypoxia contributes to plaque inflammation and growth. Disturbed blood flow in vascular bifurcations and curvatures leads to reduced oxygen transport from blood to the inner layers of the wall and contributes to the development of atherosclerotic plaques in these regions. Recent studies have shown that hypoxia-inducible factor-1α (HIF-1α), a critical transcription factor associated with hypoxia, is also activated in disturbed flow by a mechanism that is independent of hypoxia. A final section of the review emphasizes hypoxia in vascular stenting that is used to enlarge vessels occluded by plaques. Stenting can compress the VV leading to hypoxia and associated intimal hyperplasia. To enhance oxygen transport during stenting, new stent designs with helical centrelines have been developed to increase blood phase oxygen transport rates and reduce intimal hyperplasia. Further study of the mechanisms controlling hypoxia in the artery wall may contribute to the development of therapeutic strategies for vascular diseases.

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