Shear rate dependent margination of sphere-like, oblate-like and prolate-like micro-particles within blood flow

Soft Matter ◽  
2018 ◽  
Vol 14 (36) ◽  
pp. 7401-7419 ◽  
Author(s):  
Huilin Ye ◽  
Zhiqiang Shen ◽  
Ying Li
Keyword(s):  
Blood Flow ◽  
Shear Rate ◽  
Shape Effect ◽  
Shear Rates ◽  
Micro Particles ◽  
Rate Dependent ◽  
Wall Shear

The shape effect of micro-particles is examined by comparing the margination behaviors of sphere-like, oblate-like and prolate-like micro-particles under different wall shear rates in blood flow.

Adenosine Diphosphate-Induced Aggregation of Human Platelets in Flow Through Tubes: III. Shear and Extrinsic Fibrinogen-Dependent Effects

1994 ◽  
Vol 71 (01) ◽  
pp. 078-090 ◽  
Author(s):  
H L Goldsmith ◽  
M M Frojmovic ◽  
Susan Braovac ◽  
Fiona McIntosh ◽  
T Wong
Keyword(s):  
Shear Rate ◽  
Single Cells ◽  
Adenosine Diphosphate ◽  
Human Platelets ◽  
Size Analysis ◽  
Fibrinogen Concentration ◽  
Human Fibrinogen ◽  
Shear Rates ◽  
Rate Dependent ◽  
Induced Aggregation

SummaryThe effect of shear rate and fibrinogen concentration on adenosine diphosphate-induced aggregation of suspensions of washed human platelets in Poiseuille flow at 23°C was studied using a previously described double infusion technique and resistive particle counter size analysis (1). Using suspensions of multiple-centrifuged and -washed cells in Tyrodes-albumin [3 × 105 μl−1; (17)] with [fibrinogen] from 0 to 1.2μM, the, rate and extent of aggregation with 0.7 μM ADP in Tyrodes-albumin were measured over a range of mean transit times from 0.2 to 43 s, and at mean tube shear rates, Ḡ, = 41.9, 335 and 1,335 s−1. As measured by the decrease in singlet concentration, aggregation at 1.2 μM fibrinogen increased with increasing Ḡ up to 1,335 s1, in contrast to that previously reported in citratcd plasma, in which aggregation reached a maximum at Ḡ = 335 s−1. Without added fibrinogen, there was no aggregation at Ḡ = 41.9 s1; at Ḡ = 335 s1, there was significant aggregation but with an initial lag time, aggregation increasing further at Ḡ = 1,335 s−1. Without added fibrinogen, aggregation was abolished at all Ḡ upon incubation with the hexapeptide GRGDSP, but was almost unaffected by addition of an F(ab’)2 fragment of an antibody to human fibrinogen. Aggregation in the absence of added fibrinogen was also observed at 37°C. The activation of the multiple-washed platelets was tested using flow cytometry with the fluorescently labelled monoclonal antibodies FITC-PAC1 and FITC-9F9. It was shown that 57% of single cells in unactivated PRT expressed maximal GPIIb-IIIa fibrinogen receptors (MoAb PAC1) and 54% expressed pre-bound fibrinogen (MoAb 9F9), with further increases on ADP activation. However, incubation with GRGDSP and the F(ab’)2 fragment did not inhibit the prebound fibrinogen. Moreover, relatively unactivated cells (8% expressing receptor, 14% prebound fibrinogen), prepared from acidified cPRP by single centrifugation with 50 nM of the stable prostacyclin derivative, ZK 36 374, and resuspension in Tyrodes-albumin at 5 × 104 μl−1, aggregated with 2 and 5 μM ADP at Ḡ = 335 and 1,335 s−1 in the absence of added fibrinogen. We therefore postulate that a protein such as von Willebrand factor, secreted during platelet isolation or in flow at sufficiently high shear rates, may yield the observed shear-rate dependent aggregation without fibrinogen.

scholarly journals Von Willebrand factor in the vessel wall mediates platelet adherence

Blood ◽  
1985 ◽  
Vol 65 (1) ◽  
pp. 85-90 ◽  
Author(s):  
HV Stel ◽  
KS Sakariassen ◽  
PG de Groot ◽  
JA van Mourik ◽  
JJ Sixma
Keyword(s):  
Monoclonal Antibody ◽  
Shear Rate ◽  
Von Willebrand Factor ◽  
Vessel Wall ◽  
Human Artery ◽  
Shear Rates ◽  
Platelet Adherence ◽  
Wall Shear ◽  
Von Willebrand ◽  
Willebrand Factor

Abstract A monoclonal antibody directed against the von Willebrand factor moiety (vWF) of factor VIII-von Willebrand factor (FVIII-vWF), which blocks ristocetin-induced platelet aggregation as well as the binding of FVIII- vWF to platelets in the presence of ristocetin, inhibited platelet adherence to human artery subendothelium when present in normal flowing blood. This monoclonal antibody, CLB-RAg 35, inhibited platelet adherence as a function of the shear rate. At wall shear rates below 500 s-1, platelet adherence was not affected, but at higher shear rates platelet adherence was gradually inhibited, reaching an average of 11% of the normal value at 2,500 s-1. Indirect immunofluorescence established the reactivity of CLB-RAg 35 with vWF present in artery subendothelium. Pretreatment of normal vessel walls with this antibody inhibited adherence of platelets in blood from a patient with severe homozygous von Willebrand's disease and in blood from normal individuals. The inhibition was shear-rate dependent and significant at high shear rates (2,500 s-1). By adding increasing amounts of purified FVIII-vWF to normal blood, the inhibition was gradually overcome. These data indicate that vWF present in the vessel wall contributes appreciably to platelet adherence. At high wall shear rates, platelet adherence is mediated virtually completely by both plasma FVIII-vWF and vWF in the vessel wall. At low wall shear rates (below 500 s-1), platelet adherence occurs independent of FVIII-vWF in plasma and vWF in the vessel wall.

scholarly journals Platelet adhesion to collagen types I through VIII under conditions of stasis and flow is mediated by GPIa/IIa (alpha 2 beta 1-integrin)

Blood ◽  
1994 ◽  
Vol 83 (5) ◽  
pp. 1244-1250 ◽  
Author(s):  
EU Saelman ◽  
HK Nieuwenhuis ◽  
KM Hese ◽  
PG de Groot ◽  
HF Heijnen ◽  
...  
Keyword(s):  
Shear Rate ◽  
Platelet Adhesion ◽  
Collagen Type ◽  
Divalent Cations ◽  
Collagen Types ◽  
Shear Rates ◽  
Rate Dependent ◽  
Platelet Receptor ◽  
Static Conditions ◽  
Type V

Abstract Platelet adhesion to fibrillar collagens (types I, II, III, and V) and nonfibrillar collagens (types IV, VI, VII, and VIII) was investigated in the presence of physiologic concentrations of divalent cations under conditions of stasis and flow. Under static conditions, platelet adhesion was observed to collagen types I through VII but not to type VIII. Under flow conditions, platelet adhesion to collagen types I, II, III, and IV was almost independent of shear rates above 300/s. Collagen type V was nonadhesive. Platelet adhesion to collagen type VI was shear rate-dependent and optimal at a rate of 300/s. Collagen types VII and VIII showed minor reactivity and supported platelet adhesion only between shear rates 100 to 1,000/s. Monoclonal antibody (MoAb) 176D7, directed against platelet membrane glycoprotein Ia (GPIa; very late antigen [VLA]-alpha 2 subunit), completely inhibited platelet adhesion to all collagens tested, under conditions of both stasis and flow. Platelet adhesion to collagen type III at shear rate 1,600/s was only inhibited for 85%. The concentration of antibody required for complete inhibition of platelet adhesion was dependent on the shear rate and the reactivity of the collagen. An MoAb directed against GPIIa (VLA-beta subunit) partially inhibited platelet adhesion to collagen. These results show that GPIa-IIa is a major and universal platelet receptor for eight unique types of collagen.

Therapeutic Amelioration of Vaso-Occlusion and Blood Flow Impairment in Transgenic Sickle Mice By the Antioxidant Flavonoid Quercetin

Blood ◽  
2014 ◽  
Vol 124 (21) ◽  
pp. 4054-4054
Author(s):  
Sangeetha Thangaswamy ◽  
Henny H Billett ◽  
Craig A. Branch ◽  
Sandra M. Suzuka ◽  
Seetharama A Acharya
Keyword(s):  
Blood Flow ◽  
Shear Rate ◽  
Leukocyte Adhesion ◽  
Flow Direction ◽  
Radical Scavenging ◽  
Wall Shear Rate ◽  
Cremaster Muscle ◽  
Wild Type ◽  
Wall Shear

Abstract Sickle cell disease (SCD) is characterized by painful vaso-occlusive crises, which are, at least in part, due to an interaction of the sickle RBC (sRBC) with the vascular endothelium. Abnormal red blood cells (RBCs) impair blood flow and contribute to microcirculatory complications. Oxidative stress and/or oxidants generated via hemoglobin S (HbS) auto-oxidation play a vital role in the vaso-occlusive event in SCD. Antioxidant therapy mediated free radical scavenging and attenuation of oxidative stress may reduce red cell sickling and be beneficial for SCD. Several studies have described an antioxidant effect of flavonoids on the attenuation of free radical mediated biological membrane damage and the consumption of flavonoids reduces the prevalence of vascular diseases. Among flavonoids, quercetin (QUE) pentahydroxy flavone is the major representative. In vitro, QUE is a strong antioxidant with alkoxyl and peroxy radical scavenging ability. Due to the high susceptibility of sickle RBC to oxidation, QUE could be a useful therapy for SCD. Based on this concept, we examined the potential effect of QUE to improve microvascular function in a murine model of SCD. Methods: To confirm the protective effect of quercetin in vivo, we used Berkeley (Berk) sickle transgenic mice which express exclusively human α- and βS-globins with low levels of γ-globin (∼ 3-5%) generated by Paszty et al 1997. C57BL /6J were used as control wild type. We injected a single dose of QUE at different concentrations (50, 100, 200mg/kg body weight) intraperitoneally under normoxic conditions. Three hours after QUE administration, in vivo intra-vital microscopic observation of post-capillary venules in cremaster muscle was performed. The luminal diameters of the venules (∼ 20-40 µm diameter), centerline red blood cell velocity (Vrbc), adherent, emigrated and rolling leukocytes were measured by the technique described by Kaul et al 2004. Wall shear rate was calculated by Lipowsky et al, 1980. Results: QUE treatment restored blood flow, as evidenced by complete disappearance of vaso-occlusion in the postcapillary venules of Berk mice (Figure 1). However, no significant differences in venular diameter were noted with QUE treatment at any of the dose levels tested (50, 100, 200mg/kg) when compared to untreated Berk and wild type mice. But, when compared to untreated Berk mice, a significant increase in the RBC velocity was demonstrated in a dose dependent fashion (treated: 1.74 ±1.3 mm/sec, 3.02± 1.2 mm/sec, 3.4±0.90 mm/sec for 50, 100, 200 mg/kg dosing respectively vs. untreated 1.01± 1.05mm/sec, p<0.05). A dose of 200 mg level completely neutralized the vaso-occlusion. Increases in wall shear rate (650.01± 252.05 s-1 vs. 180.12± 165.02 s-1, p<6.03x10-6) was also observed in QUE treated vs. untreated Berk. This improvement of blood flow in the postcapillary venules correlated well with observed decreases in leukocyte adhesion (Figure 2A) and leukocyte emigration (Figure 2B) in QUE treated Berk mice (for doses 50, 100, and 200mg/kg) when compared to untreated Berk mice. Leukocyte rolling was also decreased for doses 100 and 200mg/kg (p<0.007, p<0.0002 respectively) after treatment with QUE when compared to untreated Berk and wild type. Figure 1: Representative images showing postcapillary venules in the cremaster muscle microcirculation of Berk mice compared to QUE treated and wild type. Black arrows indicate leukocytes and white arrows indicate the blood flow direction. Figure 1:. Representative images showing postcapillary venules in the cremaster muscle microcirculation of Berk mice compared to QUE treated and wild type. Black arrows indicate leukocytes and white arrows indicate the blood flow direction. Figure 2: Leukocyte adhesion (2A) and emigration (2B) in QUE treated Berk mice at 50, 100 and 200mg/kg doses compared to untreated Berk and wild type. Figure 2:. Leukocyte adhesion (2A) and emigration (2B) in QUE treated Berk mice at 50, 100 and 200mg/kg doses compared to untreated Berk and wild type. Figure 3 Figure 3. Conclusion: We observed an improvement in RBC velocity and wall shear rate, as well as a complete attenuation of leukocyte adhesion, rolling and emigration at the highest dose of QUE treated transgenic sickle Berk mice. We suggest that these effects may be due to a decreased sickle RBC interaction with the vascular bed. Our present data provide a strong basis for the therapeutic application of flavonoids in SCD. Further studies are needed to better understand the mechanism of action in vivo for therapeutic effect in SCD. Disclosures Thangaswamy: AMI Life Sciences Private Ltd: Drug supplied Other. Billett:Selexys Pharmaceuticals: Research Funding.

A Scaling Law for Wall Shear Rate Through an Arterial Stenosis

1994 ◽  
Vol 116 (4) ◽  
pp. 446-451 ◽  
Author(s):  
John M. Siegel ◽  
Christos P. Markou ◽  
David N. Ku ◽  
S. R. Hanson
Keyword(s):  
Shear Rate ◽  
Plaque Rupture ◽  
Scaling Law ◽  
Wall Shear Rate ◽  
Arterial System ◽  
Arterial Stenosis ◽  
Atheromatous Plaque ◽  
High Grade ◽  
Shear Rates ◽  
Wall Shear

Atherosclerosis of the human arterial system produces major clinical symptoms when the plaque advances to create a high-grade stenosis. The hemodynamic shear rates produced in high-grade stenoses are important in the understanding of atheromatous plaque rupture and thrombosis. This study was designed to quantify the physiologic stress levels experienced by endothelial cells and platelets in the region of vascular stenoses. The steady hemodynamic flow field was solved for stenoses with percent area reductions of 50, 75, and 90 percent over a range of physiologic Reynolds numbers (100–400). The maximum wall shear rate in the throat region can be shown to vary by the square root of the Reynolds number. The shear rate results can be generalized to apply to a range of stenosis lengths and flow rates. Using dimensions typical for a human carotid or coronary artery, wall shear rates were found to vary from a maximum of 20,000 s−1 upstream of the throat to a minimum of −630 s−1 in the recirculation zone for a 90 percent stenosis. An example is given which illustrates how these values can be used to understand the relationship between hemodynamic shear and platelet deposition.

Derivation of Shear Rates From Near-Wall LDA Measurements Under Steady and Pulsatile Flow Conditions

1994 ◽  
Vol 116 (3) ◽  
pp. 361-368 ◽  
Author(s):  
Ray S. Fatemi ◽  
Stanley E. Rittgers
Keyword(s):  
Shear Rate ◽  
Linear Approximation ◽  
Curve Fitting ◽  
Pulsatile Flow ◽  
Wall Shear Rate ◽  
Measured Velocity ◽  
Shear Rates ◽  
Wall Shear ◽  
Flow Waveforms ◽  
Near Wall

Atherosclerosis, thrombosis, and intimal hyperplasia are major forms of cardiovascular diseases in the United States. Previous studies indicate a significant correlation between hemodynamics, in particular, wall shear rate, and pathology of the arterial walls. While results of these studies implicate morphologic and functional changes related to wall shear rate magnitude, a standard technique for wall shear rate measurement has not been established. In this study, theoretical and in-vitro experimental fully developed steady and physiologic pulsatile flow waveforms have been used to obtain velocity profiles in the near-wall region. The estimated wall shear rates from these results are compared to the theoretical value to assess the accuracy of the approximating technique. Experimentally obtained results from LDA suggest that in order to minimize the error in velocity data, and subsequently, the wall shear rate, the first measured velocity has to be 500 μm away from the wall. While a linear approximation did not produce errors larger than 16.4 percent at peak systole, these errors substantially increased as the velocity magnitudes decreased during late systole and diastole. Overall, a third degree polynomial curve fit using four points produced the most accurate estimation of wall shear rate through out the cardiac cycle. Results of higher degree curve-fitting functions can be unpredictable due to potential oscillations of the function near the wall. Hence, based on the results of this study, use of a linear approximation is not recommended; a third degree curve-fitting polynomial, using four points provided the most accurate approximation for these flow waveforms.

Direct Measurement of Slip Velocities Using Three-Dimensional Total Internal Reflection Velocimetry

2005 ◽  
Author(s):  
Peter Huang ◽  
Jeffrey Guasto ◽  
Kenneth Breuer
Keyword(s):  
Shear Rate ◽  
Total Internal Reflection ◽  
Three Dimensional ◽  
Surface Hydrophobicity ◽  
Internal Reflection ◽  
Boundary Slip ◽  
Shear Rates ◽  
Rate Dependent ◽  
Close Proximity ◽  
Low Shear

The possible existence of slip of liquids in close proximity to a smooth surface is studied experimentally via the dynamics of small particles suspended in a shear flow. Sub-micron fluorescent particles suspended in water are imaged and analyzed using Total Internal Reflection Velocimetry (TIRV). For water flowing over a hydrophilic surface, the measurements are in agreement with previous experiments and indicate that slip, if present, is minimal at low shear rates, but increases slightly as the shear rate increases. Furthermore, surface hydrophobicity can be attributed for additional shear-rate dependent boundary slip. Issues associated with the experimental technique and the interpretation of results are also discussed.

scholarly journals Von Willebrand factor in the vessel wall mediates platelet adherence

Blood ◽  
1985 ◽  
Vol 65 (1) ◽  
pp. 85-90 ◽  
Author(s):  
HV Stel ◽  
KS Sakariassen ◽  
PG de Groot ◽  
JA van Mourik ◽  
JJ Sixma
Keyword(s):  
Monoclonal Antibody ◽  
Shear Rate ◽  
Von Willebrand Factor ◽  
Vessel Wall ◽  
Human Artery ◽  
Shear Rates ◽  
Platelet Adherence ◽  
Wall Shear ◽  
Von Willebrand ◽  
Willebrand Factor

A monoclonal antibody directed against the von Willebrand factor moiety (vWF) of factor VIII-von Willebrand factor (FVIII-vWF), which blocks ristocetin-induced platelet aggregation as well as the binding of FVIII- vWF to platelets in the presence of ristocetin, inhibited platelet adherence to human artery subendothelium when present in normal flowing blood. This monoclonal antibody, CLB-RAg 35, inhibited platelet adherence as a function of the shear rate. At wall shear rates below 500 s-1, platelet adherence was not affected, but at higher shear rates platelet adherence was gradually inhibited, reaching an average of 11% of the normal value at 2,500 s-1. Indirect immunofluorescence established the reactivity of CLB-RAg 35 with vWF present in artery subendothelium. Pretreatment of normal vessel walls with this antibody inhibited adherence of platelets in blood from a patient with severe homozygous von Willebrand's disease and in blood from normal individuals. The inhibition was shear-rate dependent and significant at high shear rates (2,500 s-1). By adding increasing amounts of purified FVIII-vWF to normal blood, the inhibition was gradually overcome. These data indicate that vWF present in the vessel wall contributes appreciably to platelet adherence. At high wall shear rates, platelet adherence is mediated virtually completely by both plasma FVIII-vWF and vWF in the vessel wall. At low wall shear rates (below 500 s-1), platelet adherence occurs independent of FVIII-vWF in plasma and vWF in the vessel wall.

scholarly journals Glycoprotein Ib, von Willebrand factor, and glycoprotein IIb:IIIa are all involved in platelet adhesion to fibrin in flowing whole blood

Blood ◽  
1990 ◽  
Vol 76 (2) ◽  
pp. 345-353 ◽  
Author(s):  
RR Hantgan ◽  
G Hindriks ◽  
RG Taylor ◽  
JJ Sixma ◽  
PG de Groot
Keyword(s):  
Platelet Aggregation ◽  
Shear Rate ◽  
Von Willebrand Factor ◽  
Whole Blood ◽  
Platelet Adhesion ◽  
Thrombus Formation ◽  
Shear Rates ◽  
Wall Shear ◽  
Von Willebrand ◽  
Willebrand Factor

We have investigated the molecular basis of thrombus formation by measuring the extent of platelet deposition from flowing whole blood onto fibrin-coated glass coverslips under well-defined shear conditions in a rectangular perfusion chamber. Platelets readily and specifically adhered to fibrin-coated coverslips in 5 minute perfusion experiments done at either low (300 s-1) or high (1,300 s-1) wall shear rates. Scanning electron microscopic examination of fibrin-coated coverslips after perfusions showed surface coverage by a monolayer of adherent, partly spread platelets. Platelet adhesion to fibrin was effectively inhibited by a monoclonal antibody (MoAb) specific for glycoprotein (GP) IIb:IIIa. The dose-response curve for inhibition of adhesion by anti-GPIIb:IIIa at both shear rates paralleled that for inhibition of platelet aggregation. Platelet aggregation and adhesion to fibrin were also blocked by low concentrations of prostacyclin. In contrast, anti- GPIb reduced adhesion by 40% at 300 s-1 and by 70% at 1,300 s-1. A similar pattern of shear rate-dependent, incomplete inhibition resulted with a MoAb specific for the GPIb-recognition region of von Willebrand factor (vWF). Platelets from an individual with severe von Willebrand's disease, whose plasma and platelets contained essentially no vWF, exhibited defective adhesion to fibrin, especially at the higher shear rate. Addition of purified vWF restored adhesion to normal values. These results are consistent with a two-site model for platelet adhesion to fibrin, in which the GPIIb:IIIa complex is the primary receptor, with GPIb:vWF providing a secondary adhesion pathway that is especially important at high wall shear rates.

scholarly journals Effect of blood flow on thrombin generation is dependent on the nature of the thrombogenic surface

Blood ◽  
1994 ◽  
Vol 84 (7) ◽  
pp. 2206-2213 ◽  
Author(s):  
A Diquelou ◽  
S Lemozy ◽  
D Dupouy ◽  
B Boneu ◽  
K Sakariassen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Blood Flow ◽  
Shear Rate ◽  
Plasma Levels ◽  
Thrombin Generation ◽  
Type Iii Collagen ◽  
Fibrin Deposition ◽  
Positive Correlation ◽  
Shear Rates ◽  
Fibrin Formation

We have investigated the influence of blood flow on thrombin generation, fibrin formation, and fibrin deposition on procoagulant and nonprocoagulant surfaces. Nonanticoagulated human blood was drawn for 5 minutes directly from an antecubital vein over stimulated endothelial cells expressing tissue factor and over human type III collagen fibrils, positioned in parallel-plate perfusion chambers. The shear rates at these surfaces were 50, 650, and 2,600 s-1. Deposition of platelets and fibrin was measured by morphometry. Thrombin and fibrin formation was determined by measuring prothrombin fragments 1 + 2 (F 1 + 2), thrombin-antithrombin III complexes, (T-AT) and fibrinopeptide A (FPA) in blood effluent from the perfusion chamber at the end of the 5- minute perfusion period. On procoagulant endothelial cells, the thrombi were primarily composed of fibrin. The fibrin deposition (81%, 21%, and 2% at 50, 650, and 2,600 s-1, respectively) and plasma levels of F 1 + 2, T-AT and FPA were shear rate dependent and highest at 50 s-1. There was a positive correlation between F 1 + 2 and T-AT and the fibrin deposition (P < .01). In contrast, the collagen surface triggered primarily thrombi that were composed of platelets. The platelet thrombi and plasma levels of F 1 + 2 and T-AT were also dependent on the shear rate, but highest at 650 and 2,600 s-1. F 1 + 2 and T-AT reached the same level as observed with procoagulant endothelial cells at the higher shear rates. There was a positive correlation between F 1 + 2 and T-AT and the platelet thrombus formation (P < .05), confirming the predominant role of platelets in thrombin generation. Thus, thrombin formation is strongly influenced by the blood flow, and this effect depends on the composition of the thrombogenic surface.

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