scholarly journals Bioactive Stent Surface Coating That Promotes Endothelialization while Preventing Platelet Adhesion

2011 ◽  
Vol 12 (3) ◽  
pp. 533-539 ◽  
Author(s):  
Steven R. Meyers ◽  
Daniel J. Kenan ◽  
Xiaojuan Khoo ◽  
Mark W. Grinstaff
Keyword(s):  
Surface Coating ◽  
Platelet Adhesion ◽  
Stent Surface ◽  
Bioactive Stent

scholarly journals Preliminary study of thrombogenicity induced by the nanoparticle surface coating of intracranial stents

2019 ◽  
pp. 404-410
Author(s):  
A. Chiriac ◽  
Georgiana Ion ◽  
G. Stan ◽  
T. Popescu ◽  
Mihaela Sofronie ◽  
...  
Keyword(s):  
Surface Coating ◽  
Surface Coatings ◽  
In Vitro Tests ◽  
Thromboembolic Complications ◽  
Coagulation Time ◽  
Plasma Coagulation ◽  
Nanoparticle Surface ◽  
Preliminary Study ◽  
Stent Surface

Endovascular treatment of intracranial aneurysms with intracranial stents was proven to be clinically safe and effective, but is still associated with a risk of thromboembolic complications. Stent thrombosis could be a sever complication associated with specific stent surface coatings and designs. Standardized in vitro tests for investigation of thrombogenicity induced by different nanomaterials were used as the basic method in carrying out the present study. Therefore, the aim of this study was to evaluate the thrombogenicity of three different nanomaterials (ZnO, TiO2 si Fe3O4) possible used as surface coating for intracranial stents. This study is based on a procedure for in vitro analyses of plasma coagulation time. To measure the plasma coagulation time, platelet-poor plasma from human whole blood was in vitro exposed to nanoparticles and analysed in prothrombin (PT) and activated partial thromboplastin (APTT).

Sirolimus coating on heparinized stents prevents restenosis and thrombosis

2017 ◽  
Vol 31 (10) ◽  
pp. 1337-1345 ◽  
Author(s):  
In-Ho Bae ◽  
Kyung Seob Lim ◽  
Dae Sung Park ◽  
Jae-Won Shim ◽  
So-Youn Lee ◽  
...  
Keyword(s):  
Animal Studies ◽  
Glycolic Acid ◽  
Platelet Adhesion ◽  
Inhibitory Effect ◽  
Bare Metal Stent ◽  
Metal Stent ◽  
Stent Group ◽  
Adhesion Mechanism ◽  
Bare Metal Stent Group ◽  
Stent Surface

The aim of this study was to evaluate the inhibitory effect of sirolimus coating on the occurrence of restenosis and thrombosis with heparinized stents. Heparin and dopamine were conjugated by chemical bonding and anchored on the stent surface by a mussel-inspired adhesion mechanism. Subsequently, sirolimus was coated with poly lactic-glycolic acid on the heparinized stent surface. The heparin was well attached to the surface, and the surface was smooth after sirolimus coating. The smoothness of the surface was maintained after expansion of the stent. The amount of sirolimus released from the stent was 67.3% ± 4.55% within 7 days, followed by continual release up to day 28. The proliferation of smooth muscle cells was successfully arrested (51.3% ± 2.25% at 7 days of culture) by sirolimus released from the stent. Platelet adhesion was clearly prevented in the heparin-coated group (78.0 ± 8.00/1.8 cm2) compared to that in the heparin noncoated group (5.0 ± 1.00/1.8 cm2). Animal studies showed that the heparin and sirolimus-coated stent group had no obvious inflammatory response and no change in the fibrin score compared to those in the other groups. However, restenosis clearly decreased in the heparin and sirolimus-coated group (12.3% ± 3.54%) compared to the bare-metal stent group (27.5% ± 8.52%) and the heparin-coated group (25.3% ± 11.79%). These results suggest that heparinized surface-based sirolimus coating may be a useful approach for the prevention of restenosis and stent thrombosis.

Fine Structure of Platelet Interaction with a New Microcrystalline Collagen Preparation

1974 ◽  
Vol 32 ◽  
pp. 58-59
Author(s):  
W. H. Zucker ◽  
R. G. Mason
Keyword(s):  
Fine Structure ◽  
Platelet Aggregation ◽  
Hydrochloric Acid ◽  
Whole Blood ◽  
Platelet Adhesion ◽  
Hemostatic Agent ◽  
Native Collagen ◽  
Fibrillar Morphology ◽  
Clinical Interest ◽  
New Form

Platelet adhesion initiates platelet aggregation and is an important component of the hemostatic process. Since the development of a new form of collagen as a topical hemostatic agent is of both basic and clinical interest, an ultrastructural and hematologic study of the interaction of platelets with the microcrystalline collagen preparation was undertaken.In this study, whole blood anticoagulated with EDTA was used in order to inhibit aggregation and permit study of platelet adhesion to collagen as an isolated event. The microcrystalline collagen was prepared from bovine dermal corium; milling was with sharp blades. The preparation consists of partial hydrochloric acid amine collagen salts and retains much of the fibrillar morphology of native collagen.

Von Willebrand disease and Weibel-Palade bodies

2010 ◽  
Vol 30 (03) ◽  
pp. 150-155 ◽  
Author(s):  
J. W. Wang ◽  
J. Eikenboom
Keyword(s):  
Platelet Adhesion ◽  
Coagulation Factor ◽  
Von Willebrand Disease ◽  
Inflammatory Factors ◽  
Limited Data ◽  
Storage Organelle ◽  
And Function ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryVon Willebrand factor (VWF) is a pivotal haemostatic protein mediating platelet adhesion to injured endothelium and carrying coagulation factor VIII (FVIII) in the circulation to protect it from premature clearance. Apart from the roles in haemostasis, VWF drives the formation of the endothelial cell specific Weibel-Palade bodies (WPBs), which serve as a regulated storage of VWF and other thrombotic and inflammatory factors. Defects in VWF could lead to the bleeding disorder von Willebrand disease (VWD).Extensive studies have shown that several mutations identified in VWD patients cause an intracellular retention of VWF. However, the effects of such mutations on the formation and function of its storage organelle are largely unknown. This review gives an overview on the role of VWF in WPB biogenesis and summarizes the limited data on the WPBs formed by VWD-causing mutant VWF.

Inhibition of Platelet Adhesion to Fibrin(ogen) in Flowing Whole Blood by Arg-Gly-Asp and Fibrinogen γ-Chain Carboxy Terminal Peptides

1992 ◽  
Vol 68 (06) ◽  
pp. 694-700 ◽  
Author(s):  
Roy R Hantgan ◽  
Silvia C Endenburg ◽  
I Cavero ◽  
Gérard Marguerie ◽  
André Uzan ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Whole Blood ◽  
Platelet Adhesion ◽  
Integrin Receptor ◽  
Shear Rates ◽  
Perfusion Chamber ◽  
Receptor Recognition ◽  
Adhesive Interactions ◽  
Coated Surfaces ◽  
Carboxy Terminal

SummaryWe have employed synthetic peptides with sequences corresponding to the integrin receptor-recognition regions of fibrinogen as inhibitors of platelet aggregation and adhesion to fibrinogen-and fibrin-coated surfaces in flowing whole blood, using a rectangular perfusion chamber at wall shear rates of 300 s–1 and 1,300 s–1. D-RGDW caused substantial inhibition of platelet aggregation and adhesion to fibrinogen and fibrin at both shear rates, although it was least effective at blocking platelet adhesion to fibrin at 300 s–1. RGDS was a weaker inhibitor, and produced a biphasic dose-response curve; SDRG was inactive. HHLGGAK-QAGDV partially inhibited platelet aggregation and adhesion to fibrin(ogen) at both shear rates. These results support the identification of an RGD-specific receptor, most likely the platelet integrin glycoprotein IIb: III a, as the primary receptor responsible for platelet: fibrin(ogen) adhesive interactions under flow conditions, and indicate that platelet adhesion to surface bound fibrin(ogen) is stabilized by multivalent receptor-ligand contacts.

Platelet Adhesion to Native Collagens Involves Proteoglycans and May Be a Two-Step Process

1987 ◽  
Vol 58 (02) ◽  
pp. 786-789 ◽  
Author(s):  
O Behnke
Keyword(s):  
Electron Microscope ◽  
Platelet Adhesion ◽  
Close Contact ◽  
Blood Platelets ◽  
Collagen Fibrils ◽  
Platelet Membrane ◽  
Step Process ◽  
Rat Blood ◽  
Wide Gap ◽  
Rat Tail

SummaryAdhesion of rat blood platelets to native rat tail collagen fibrils was studied in the electron microscope under conditions that preserved collagen-associated proteoglycans (CAPG). The CAPG molecules were aligned in chain-like configurations that encircled the fibrils with a 65 nm period; they appeared to coat the fibrils completely and extended 60-100 nm away from the fibril. The initial platelet-fibril contact occurred between the platelet glycocalyx and the CAPG of the fibrils i.e. between two surfaces with net-negative charges. When close contact was established between the fibril surface proper and the platelet membrane, CAPG were not identified in the area of contact, and the collagen-platelet distance was reduced to a ~10-12 nm wide gap traversed by delicate links in register with fibril periodicities.

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