Platelets, Surfaces and Plasma Proteins in Platelet Adhesion

2015 ◽  
pp. 15-26 ◽  
Author(s):  
H. L. Nossel
1975 ◽  
Author(s):  
E. Nyilas ◽  
T.-H. Chiu ◽  
W. A. Morton ◽  
D. M. Lederman ◽  
G. A. Herzlinger ◽  
...  

To highlight the mechanisms of artificial surface/protein/platelet interactions, results obtained by various methods have been integrated to elucidate some of the correlations between phenomena which occur at the macromolecular level and subsequently influence those at the cellular level, such as platelet adhesion. Microcinematographic evidence obtained under the controlled conditions of the Stagnation Point Flow Experiment (SPFE) indicate that, even on glass, platelet adhesion commences only after 30-60 sees of exposure to native blood. This lag period is consistent with diffusion kinetics predicting the arrival of plasma proteins should overhwelmingly precede that of the cellular components. During the lag period, native plasma proteins collide with the artificial surface and, in most cases, adsorb with surface-induced conformational changes. The energy for altering the secondary protein structure is supplied by the heat of adsorption. The extent of adsorption and structural alterations depend upon both the type of protein and the molecular architecture of the artificial surface, viz., the number density and orientation of polar, H-bonding, etc. groups accessible to proteins. Using microparticulate glass (< μ dia.) and a microcalorimeter sensitive to ±0.00001° C in 100 ml of sample volume, serum albumin was found to adsorb, release heat, and desorb in a conformationally altered state. In contrast, γ-(7S)-globulin and fibrinogen underwent irreversible multilayer attachment releasing (1.0-1.7) χ 103 Kcal/mole of protein adsorbed directly to the glass surface. Proteins in the second, etc. sorbed layers released much smaller heats. The electrophoretic mobility of the same particles coated with varying amounts of the same proteins confirmed that the relatively greatest conformational change occurred in the protein layer directly attached to the artificial surface. On homologous Nylons exposed under identical hemodynamic conditions in the SPFE, the surface number density of platelets remaining adherent at points of identical shear was proportionate to the polar force contribution of those surfaces. These results indicate that the protein layer which settles first, is acting as a “proportional transformer” mediating the effects of artificial surfaces onto platelets.


Author(s):  
Linda J. Miller ◽  
Raymond T. Greer

Although there is considerable debate concerning the exact sequence of events that occur when blood contacts a foreign surface such as a polymer, most investigators agree on the basic sequence: polymer surfaceblood contact, competitive adsorption of plasma proteins, formation of protein coated surface, platelet approach, platelet reaction with glycoproteins, platelet adhesion, thrombus and coagulation.


1981 ◽  
Author(s):  
O P Malhotra ◽  
M N Helmus ◽  
D F Gibbons

On occasion, fewer platelets from platelet rich plasma (PRP), adhered to hydrophilic (glass) surfaces exposed to platelet poor plasma (PPP) for 3 min than areas exposed for 3 s. The decrease was dramatic and consistent when platelet suspension (gel-PLS, obtained from PRP by 2B Sepharose gel filtration) was used instead of PRP. To further explore the factors which influence platelet adhesion, we used the following: for surfaces, a) sparkleen-cleaned glass (hydrophilic), b) acid-washed (somewhat hydrophobic), and c) siliconized (hydrophobic); for proteins, a) PPP, b) fibrinogen (96% clottable), c) defi-brinogenated (defib.) plasma, and d) defib. plasma plus fibrinogen; for platelet suspension, a) PRP, b) gel-PLS, and c) platelets in defib. plasma (defib. PLS).From gel-PLS, non-siliconized surfaces exposed to fibrinogen for 3 s attached more platelets (F<0.05) than those exposed to PPP or defib. plasma plus fibrinogen. The latter two attracted more platelets (P<0.01) than defib. plasma. Hydrophilic sparkleen-cleaned glass previously exposed to PPP (or defib. plasma plus fibrinogen) attached a minimum of 10-fold as many platelets from gel-PLS than from PRP. Under similar conditions acid-cleaned surfaces attached 2-fold from gel-PLS, while hydrophobic glass did not show any change. By exposing the surfaces to PPP followed by gel-PLS, the sparkleen-cleaned glass showed the greatest decrease (P<0.001) in the number of platelets attached to areas exposed to PPP for 3 min as compared to 3 s, while siliconized showed no such decrease. If, however, the surfaces were exposed to defib. plasma, they all showed decreases in platelet attraction at 3 min.


2009 ◽  
Vol 79-82 ◽  
pp. 727-730 ◽  
Author(s):  
Qi Yi Wang ◽  
Ping Yang ◽  
Ju Huang ◽  
Jun Liang ◽  
Hong Sun ◽  
...  

Low hemocompatibility is a major problem of biomaterials that come in contact with blood. Surface modification has become an important way to improve the hemocompatibility of medical implants and interventional devices. Recently, researchers attempt to investigate the possibility of silicon oxynitride (Si-N-O) films to be applied as novel coating of blood-contacting biomaterials. However, no detailed investigation has been conducted. In this study, our work was focused on the optimization of the hemocompatibility of Si-N-O films prepared on single-crystal silicon wafers by unbalance magnetron sputtering (UBMS). The structure and chemical composition of films were characterized by X-ray photoelectron spectrometry (XPS), and their physical chemistry property was characterized by contact angle measurements. Platelet adhesion test was performed to investigate the platelet adhesion and activation. Our results suggested that films composed of Si3N4 and SiOx (x<2) exhibited better hemocompatibility than low temperature isotropic pyrolitic carbon (LTIC) that is a common material used in blood-contacting implants. It was also revealed that the higher N/O ratio in films composed of Si3N4 and SiOx (x<2) was attributed to the lower platelet adhesion and activation, and the interaction of samples with plasma proteins was demonstrated to play an important role in the adhesion and activation of platelets.


Biomaterials ◽  
1988 ◽  
Vol 9 (2) ◽  
pp. 138-144 ◽  
Author(s):  
Inn-Kyu Kang ◽  
Yoshihiro Ito ◽  
Masahiko Sisido ◽  
Yukio Imanishi

1989 ◽  
Vol 257 (4) ◽  
pp. H1076-H1081
Author(s):  
E. F. Ritter ◽  
R. D. Vann ◽  
C. Wyble ◽  
W. J. Barwick ◽  
B. Klitzman

A prime factor in the thrombogenicity of synthetic materials in contact with blood is the blood-gas interface. Small pockets of gas, known as gas nuclei, are trapped within surface interstices. The resulting blood-gas interface denatures plasma proteins and activates clotting factors and platelets. Expanded polytetrafluoroethylene (ePTFE) vascular prostheses 1 mm in internal diameter were placed in saline under 6,000 psig hydrostatic pressure for 2 h in an attempt to dissolve all gas nuclei (i.e., to denucleate). Carotid-carotid bypasses were performed in rats using 280-mm lengths of ePTFE. All 10 control grafts lost patency in 5 min, whereas the 14 denucleated grafts had a median patency duration of 300 min (P less than 0.01). In 15-mm-long rat femoral artery interpositional ePTFE grafts, 90% of controls thrombosed within 10 min, whereas only 7% of denucleated grafts thrombosed over the duration of the 7-day observation period (P less than 0.001). Denucleation also resulted in a significant reduction (P less than 0.02) in 111In-labeled platelet adhesion to 36% of control. Scanning electron microscopy confirmed the reduced accumulation of platelets on denucleated grafts. These data suggest that the removal of trapped air with hydrostatic pressure significantly reduces the thrombogenicity of ePTFE microvascular prostheses and may have application to other clinical (catheters, valves, tubing, etc.) or experimental (micropipettes, electrodes, etc.) materials that interface with blood.


Microbiology ◽  
2010 ◽  
Vol 156 (3) ◽  
pp. 920-928 ◽  
Author(s):  
Helen Miajlovic ◽  
Marta Zapotoczna ◽  
Joan A. Geoghegan ◽  
Steven W. Kerrigan ◽  
Pietro Speziale ◽  
...  

The interaction of bacteria with platelets is implicated in the pathogenesis of endovascular infections, including infective endocarditis, of which Staphylococcus aureus is the leading cause. Several S. aureus surface proteins mediate aggregation of platelets by fibrinogen- or fibronectin-dependent processes, which also requires specific antibodies. In this study S. aureus was grown in iron-limited medium to mimic in vivo conditions in which iron is unavailable to pathogens. Under such conditions, a S. aureus mutant lacking the known platelet-activating surface proteins adhered directly to platelets in the absence of plasma proteins and triggered aggregation. Platelet adhesion and aggregation was prevented by inhibiting expression of iron-regulated surface determinant (Isd) proteins. Mutants defective in IsdB, but not IsdA or IsdH, were unable to adhere to or aggregate platelets. Antibodies to the platelet integrin GPIIb/IIIa inhibited platelet adhesion by IsdB-expressing strains, as did antagonists of GPIIb/IIIa. Surface plasmon resonance demonstrated that recombinant IsdB interacts directly with GPIIb/IIIa.


1994 ◽  
Vol 57 (1) ◽  
pp. 133-137 ◽  
Author(s):  
L.T. DiFazio ◽  
C. Stratoulias ◽  
R.S. Greco ◽  
B. Haimovich

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