Platelet Associated Fibrinogen and ICAM-2 Induce Firm Adhesion of Neutrophils under Flow Conditions

1998 ◽  
Vol 80 (09) ◽  
pp. 443-448 ◽  
Author(s):  
P. H. M. Kuijper ◽  
H. I. Gallardo Torres ◽  
J.-W. J. Lammers ◽  
J. J. Sixma ◽  
L. Koenderman ◽  
...  

SummarySurface-bound platelets support selectin-mediated rolling and β2-integrin-mediated firm adhesion of neutrophils (PMN) under flow conditions. We examined which ligands on platelets mediate this firm adhesion. Surface-bound platelets express ICAM-2 and GPIIbIIIa-bound fibrinogen, which are ligands for LFA-1 and MAC-1. In a well defined model for vessel wall injury, blood from an afibrinogenemic patient was perfused over ECM-coated coverslips to obtain fibrinogen-free platelet surfaces. At high shear rates, PMN-adhesion to fibrinogen-free platelet surfaces decreased compared to fibrinogen-containing controls. Under these conditions, firm adhesion and not rolling was blocked demonstrating the importance of fibrinogen in this process. In addition, MAC-1 and LFA-1 on PMN and ICAM-2 on platelets played a role in firm adhesion; the effect of blocking antibodies was most evident at high shear. The effects of fibrinogen depletion and ICAM-2 blocking were additive. In conclusion, multiple redundant ligands, like ICAM-2 and fibrinogen, induce firm and shear resistant PMN adhesion to platelets under flow conditions. Individually these ligands become critical at higher shear. Blocking of two or more interactions also interferes with low shear adhesion.

1992 ◽  
Vol 289 ◽  
Author(s):  
John R. Melrose

AbstractAn overview is given of theories of aggregates under flow. These generally assume some sort of structural breakdown as the shear rate is increased. Models vary with both the rigidity of the bonding and the level of treatment of hydrodynamics. Results are presented for simulations of a Rouse model of non-rigid, (i.e. central force) weakly bonded aggregates. In large scale simulations different structures are observed at low and high shear rates. The change from one structure to another is associated with a change in the rate of shear thinning. The model captures low shear rate features of real systems absent in previous models: this feature is ascribed to agglomerate deformations. Quantitatively, the model is two orders of magnitude out from experiment but some scaling is possible.


Blood ◽  
1995 ◽  
Vol 85 (3) ◽  
pp. 705-711 ◽  
Author(s):  
J Harsfalvi ◽  
JM Stassen ◽  
MF Hoylaerts ◽  
E Van Houtte ◽  
RT Sawyer ◽  
...  

Calin from the saliva of the medicinal leech, Hirudo medicinalis, is a potent inhibitor of collagen mediated platelet adhesion and activation. In addition to inhibition of the direct platelet-collagen interaction, we presently demonstrate that binding of von Willebrand to coated collagen can be prevented by Calin, both under static and flow conditions in agreement with the occurrence of binding of Calin to collagen, confirmed by Biospecific Interaction Analysis. To define whether Calin acted by inhibiting the platelet-collagen or the platelet- von Willebrand factor (vWF)-collagen-mediated thrombus formation, platelet adhesion to different types of collagens was studied in a parallel-plate flow chamber perfused with whole blood at different shear rates. Calin dose-dependently prevented platelet adhesion to the different collagens tested both at high- and low-shear stress. The concentration of Calin needed to cause 50% inhibition of platelet adhesion at high-shear stress was some fivefold lower than that needed for inhibition of vWF-binding under similar conditions, implying that at high-shear stress, the effect of Calin on the direct platelet- collagen interactions, suffices to prevent thrombus formation. Platelet adhesion to extracellular matrix (ECM) of cultured human umbilical vein endothelial cells was only partially prevented by Calin, and even less so at a high-shear rather than a low-shear rate, whereas the platelet binding to coated vWF and fibrinogen were minimally affected at both shear rates. Thus, Calin interferes with both the direct platelet- collagen interaction and the vWF-collagen binding. Both effects may contribute to the inhibition of platelet adhesion in flowing conditions, although the former seems to predominate.


Author(s):  
Neema Nair ◽  
George M. Pantalos ◽  
M. Keith Sharp

Motivated by questions related to flow in pediatric cardiovascular devices, the purpose of this study was to compare pediatric and adult complex viscoelasticity η* = ηV − iηE, where ηV and ηE are viscous and elastic components, respectively, measured in oscillatory flow in a capillary tube [Thurston 1972]. For normal blood, viscosity is increased at low shear rates by red cell aggregation and reduced at high shear rates due to disaggregation, orientation and deformation of red cells. The elastic part is also normally psuedoplastic, indicative of the deformation of red cell aggregates at high shear and individual cells at low shear, respectively.


2007 ◽  
Vol 129 (2) ◽  
pp. 438-449 ◽  
Author(s):  
Emmanuel Y. A. Wornyoh ◽  
Venkata K. Jasti ◽  
C. Fred Higgs

Research efforts related to dry particulates in sliding contacts are reviewed. In the tribology community, there are primarily two types of dry particulate lubricants that are studied—granular and powder. Granular lubricants usually refer to dry, cohesionless, hard particles that transfer momentum and accommodate surface velocity differences through shearing and rolling at low shear rates, and collisions at high shear rates. Powder lubricants refer to dry, cohesive, soft particles that accommodate surface velocity differences mostly by adhering to surfaces and shearing in the bulk medium, in a manner similar to hydrodynamic fluids. Spanning the past five decades, this review proposes a classification system for the scientific works in the dry particulate tribology literature in terms of theory, experiments, and numerical simulations. It also suggests that these works can be further categorized based on their tribosystem geometry—annular, parallel, and converging.


Blood ◽  
1997 ◽  
Vol 89 (1) ◽  
pp. 166-175 ◽  
Author(s):  
P.H.M. Kuijper ◽  
H.I. Gallardo Torres ◽  
J.-W.J. Lammers ◽  
J.J. Sixma ◽  
L. Koenderman ◽  
...  

Abstract At sites of vessel wall damage, the primary hemostatic reaction involves platelet and fibrin deposition. At these sites, circulating leukocytes marginate and become activated. Adhered platelets can support leukocyte localization; however, the role of fibrin in this respect is not known. We studied the adhesion of human neutrophils (polymorphonuclear leukocytes [PMNs]) to endothelial extracellular matrix (ECM)-bound fibrin and platelets under flow conditions. ECM alone did not show PMN adhesion. ECM-coated cover slips were perfused with plasma to form a surface-bound fibrin network, and/or with whole blood to allow platelet adhesion. Unstimulated PMNs adhered to fibrin at moderate shear stress (20 to 200 mPa). ECM-bound platelets induced rolling adhesion and allowed more PMNs to adhere at higher shear (320 mPa). ECM coated with both platelets and fibrin induced more static and shear-resistant PMN adhesion. PMN adhesion to fibrin alone but not to platelet/fibrin surfaces was inhibited by soluble fibrinogen. Adhesion to fibrin alone was inhibited by CD11b and CD18 blocking antibodies. Furthermore, fibrin formed under flow conditions showed up to threefold higher PMN adhesion compared with fibrin formed under static conditions, due to structural differences. These results indicate that circulating PMNs adhere to fibrin in an integrin-dependent manner at moderate shear stresses. However, at higher shear rates (<200 mPa), additional mechanisms (ie, activated platelets) are necessary for an interaction of PMNs with a fibrin network.


2014 ◽  
Vol 217-218 ◽  
pp. 83-90
Author(s):  
Mehdi Reisi ◽  
Behzad Niroumand ◽  
Ebrahim Shirani

Morphological evolution of a transparent model succinonitrile (SCN) material during solidification was investigated in an apparatus resembling a shearing-disc viscometer. The in situ microscopic observations showed that fragmentation decreased the average particles size, but did not result in transition of dendritic to spherical morphology. At low shear rates, the degenerated dendrites and at high shear rates, the pseudo-cluster morphology was observed. It was revealed that coarsening has the most important effect on the final morphology of solid particles. The quantitative influences of shearing rate and intensity on the size and morphology of solid crystals were also discussed based on the measurements on the microstructures.


1976 ◽  
Vol 98 (3) ◽  
pp. 488-493 ◽  
Author(s):  
Thomas H. Reif ◽  
Robert M. Nerem ◽  
Francis A. Kulacki

The effect of high wall shear rates on the uptake of 131I-albumin by the arterial wall has been studied in vitro using common carotid arteries excised from anesthetized dogs and perfused with a steady state flow of homologous serum. Wall uptake was found to depend nearly linearly upon wall shear rate. The overall transport of 131I-albumin from the perfusing fluid to the vessel wall appears to be rate controlled by a shear dependent fluid-wall interface process. This study was carried out at high shear rates for flows which were transitional and turbulent. Because of the complexity of such flows, direct measurements of pressure drop were used to determine the shear rate at the vessel wall. Simultaneous pressure drop and flow measurements allowed the determination of the friction factor as a function of Reynolds number; results obtained at the higher Reynolds numbers correspond to those for a rigid pipe with a relative roughness of 0.05.


Blood ◽  
2002 ◽  
Vol 100 (1) ◽  
pp. 136-142 ◽  
Author(s):  
Takako Nishiya ◽  
Mie Kainoh ◽  
Mitsuru Murata ◽  
Makoto Handa ◽  
Yasuo Ikeda

Abstract Liposomes carrying both recombinant glycoprotein Ia/IIa (rGPIa/IIa) and Ibα (rGPIbα) (rGPIa/IIa-Ibα-liposomes) instantaneously and irreversibly adhered to the collagen surface in the presence of soluble von Willebrand factor (VWF) at high shear rates, in marked contrast with translocation of liposomes carrying rGPIbα alone on the VWF surface. In the absence of soluble VWF, the adhesion of rGPIa/IIa-Ibα-liposomes to the collagen surface decreased with increasing shear rates, similar to liposomes carrying rGPIa/IIa alone. While adhesion of liposomes with exofacial rGPIa/IIa and rGPIbα densities of 2.17 × 103 and 1.00 × 104molecules per particle, respectively, was efficient at high shear rates, reduction in rGPIbα density to 5.27 × 103molecules per particle resulted in decreased adhesion even in the presence of soluble VWF. A 50% reduction in the exofacial rGPIa/IIa density resulted in a marked decrease in the adhesive ability of the liposomes at all shear rates tested. The inhibitory effect of antibody against GPIbα (GUR83-35) on liposome adhesion was greater at higher shear rates. Further, the anti-GPIa antibody (Gi9) inhibited liposome adhesion more than GUR83-35 at all shear rates tested. These results suggest that the rGPIa/IIa–collagen interaction dominates the adhesion of rGPIa/IIa-Ibα-liposomes to the collagen surface at low shear rates, while the rGPIa/IIa–collagen and rGPIbα–VWF interaction complements each other, and they synergistically provide the needed functional integration required for liposome adhesion at high shear rates. This study thus has confirmed for the first time the proposed mechanisms of platelet adhesion to the collagen surface under flow conditions using the liposome system.


Blood ◽  
1997 ◽  
Vol 89 (1) ◽  
pp. 166-175 ◽  
Author(s):  
P.H.M. Kuijper ◽  
H.I. Gallardo Torres ◽  
J.-W.J. Lammers ◽  
J.J. Sixma ◽  
L. Koenderman ◽  
...  

At sites of vessel wall damage, the primary hemostatic reaction involves platelet and fibrin deposition. At these sites, circulating leukocytes marginate and become activated. Adhered platelets can support leukocyte localization; however, the role of fibrin in this respect is not known. We studied the adhesion of human neutrophils (polymorphonuclear leukocytes [PMNs]) to endothelial extracellular matrix (ECM)-bound fibrin and platelets under flow conditions. ECM alone did not show PMN adhesion. ECM-coated cover slips were perfused with plasma to form a surface-bound fibrin network, and/or with whole blood to allow platelet adhesion. Unstimulated PMNs adhered to fibrin at moderate shear stress (20 to 200 mPa). ECM-bound platelets induced rolling adhesion and allowed more PMNs to adhere at higher shear (320 mPa). ECM coated with both platelets and fibrin induced more static and shear-resistant PMN adhesion. PMN adhesion to fibrin alone but not to platelet/fibrin surfaces was inhibited by soluble fibrinogen. Adhesion to fibrin alone was inhibited by CD11b and CD18 blocking antibodies. Furthermore, fibrin formed under flow conditions showed up to threefold higher PMN adhesion compared with fibrin formed under static conditions, due to structural differences. These results indicate that circulating PMNs adhere to fibrin in an integrin-dependent manner at moderate shear stresses. However, at higher shear rates (<200 mPa), additional mechanisms (ie, activated platelets) are necessary for an interaction of PMNs with a fibrin network.


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