Faculty Opinions recommendation of Effects of paclitaxel on the ability of aspirin and clopidogrel to inhibit platelet aggregation.

2015 ◽  
Author(s):  
Davide Cattano
Keyword(s):  
Platelet Aggregation ◽  
Inhibit Platelet Aggregation

Platelet Activation and Aggregation Induced by Recombinant von Willebrand Factors Reproducing Four Type 2B von Willebrand Disease Missense Mutations

1998 ◽  
Vol 79 (01) ◽  
pp. 211-216 ◽  
Author(s):  
Lysiane Hilbert ◽  
Claudine Mazurier ◽  
Christophe de Romeuf
Keyword(s):  
Platelet Aggregation ◽  
Platelet Activation ◽  
Von Willebrand Disease ◽  
Platelet Glycoprotein ◽  
Missense Mutations ◽  
Inhibit Platelet Aggregation ◽  
Wild Type ◽  
A1 Domain ◽  
Von Willebrand ◽  
Willebrand Factor

SummaryType 2B of von Willebrand disease (vWD) refers to qualitative variants with increased affinity of von Willebrand factor (vWF) for platelet glycoprotein Ib (GPIb). All the mutations responsible for type 2B vWD have been located in the A1 domain of vWF. In this study, various recombinant von Willebrand factors (rvWF) reproducing four type 2B vWD missense mutations were compared to wild-type rvWF (WT-rvWF) for their spontaneous binding to platelets and their capacity to induce platelet activation and aggregation. Our data show that the multimeric pattern of each mutated rvWF is similar to that of WT-rvWF but the extent of spontaneous binding and the capacity to induce platelet activation and aggregation are more important for the R543Q and V553M mutations than for the L697V and A698V mutations. Both the binding of mutated rvWFs to platelets and platelet aggregation induced by type 2B rvWFs are inhibited by monoclonal anti-GPIb and anti-vWF antibodies, inhibitors of vWF binding to platelets in the presence of ristocetin, as well as by aurin tricarboxylic acid. On the other hand, EDTA and a monoclonal antibody directed against GPIIb/IIIa only inhibit platelet aggregation. Furthermore, the incubation of type 2B rvWFs with platelets, under stirring conditions, results in the decrease in high molecular weight vWF multimers in solution, the extent of which appears correlated with that of plasma vWF from type 2B vWD patients harboring the corresponding missense mutation. This study supports that the binding of different mutated type 2B vWFs onto platelet GPIb induces various degrees of platelet activation and aggregation and thus suggests that the phenotypic heterogeneity of type 2B vWD may be related to the nature and/or location of the causative point mutation.

Inhibitory Effect of Staphylokinase on Platelet Aggregation

1993 ◽  
Vol 70 (05) ◽  
pp. 834-837 ◽  
Author(s):  
Akira Suehiro ◽  
Yoshio Oura ◽  
Motoo Ueda ◽  
Eizo Kakishita
Keyword(s):  
Platelet Aggregation ◽  
Human Platelet ◽  
Degradation Products ◽  
Platelet Rich Plasma ◽  
Inhibitory Effect ◽  
Effective Concentration ◽  
Inhibit Platelet Aggregation ◽  
Platelet Suspension ◽  
Washed Platelet ◽  
Human Platelet Aggregation

SummaryWe investigated the effect of staphylokinase (SAK), which has specific thrombolytic properties, on human platelet aggregation. Platelet aggregation induced with collagen was observed following preincubation of platelets in platelet-rich plasma (PRP) or washed platelet suspension (WP) with SAK at 37° C for 30 min. SAK inhibited platelet aggregation in PRP only at the highest examined concentration (1 x 10-4 g/ml). Although SAK did not inhibit platelet aggregation in WP which contained fibrinogen, it did when the platelets had been preincubated with SAK and plasminogen. The most effective concentration in WP was 1 x 10-6 g/ml. The effect could be inhibited by adding aprotinin or α2-antiplasmin. The highest generation of plasmin in the same preincubation fluid was detected at 1 x 10-6 g/ml SAK. We concluded that SAK can inhibit platelet aggregation in WP by generating plasmin and/or fibrinogen degradation products, but is only partially effective in PRP because of the existence of α2-antiplasmin.

Maximum fluid concentrations of materials released from platelets at a surface

1983 ◽  
Vol 244 (1) ◽  
pp. H109-H114 ◽  
Author(s):  
G. A. Adams ◽  
I. A. Feuerstein
Keyword(s):  
Platelet Aggregation ◽  
Empirical Data ◽  
Maximum Amount ◽  
Inhibit Platelet Aggregation ◽  
Fluid Concentration ◽  
Diffusion And Convection ◽  
Platelet Accumulation ◽  
Von Willebrand ◽  
Willebrand Factor

We examine the estimation of local concentrations of materials that are released from the dense and alpha-granules of platelets during accumulation of platelets upon collagen-coated glass. Platelet/red blood cell suspensions were perfused through a 1.3-mm-ID tube. Empirical data were used in a calculation procedure, based on diffusion and convection, designed to yield an upper bound on the interfacial fluid concentration (IFC) for each substance considered. The necessary empirical data are the rate of platelet accumulation and the maximum amount of material in the platelet capable of secretion. It was found that the IFC is dependent on the shear rate at the surface (G) and is proportional to G0.27. This means that an eightfold increase in flow rate would increase the IFCs approximately twofold. Serotonin, pyrophosphate, adenosine 5'-monophosphate (AMP), and adenosine 5'-triphosphate (ATP) were found not to be present in sufficient quantities to produce IFCs that could influence platelet aggregation if used alone at the IFC. A second set of materials, fibrinogen, fibronectin von Willebrand factor, and calcium, had IFCs less than their concentrations normally found in plasma. A third category, containing adenosine 5'-diphosphate (ADP) alone, had an IFC close to those known to affect platelet aggregation. The role of metabolites of arachidonic acid, which may promote or inhibit platelet aggregation, awaits further description.

C0270 Analysis of different mechanisms through hydrogen sulphide (H2S) inhibit platelet aggregation

2012 ◽  
Vol 130 ◽  
pp. S103-S104
Author(s):  
Emilse Bermejo ◽  
Daniel Saenz ◽  
Maria Fabiana Alberto ◽  
Ruth Estela Rosenstein ◽  
Maria Angela Lazzari
Keyword(s):  
Platelet Aggregation ◽  
Hydrogen Sulphide ◽  
Inhibit Platelet Aggregation

Supernates from stored red blood cells inhibit platelet aggregation

Transfusion ◽  
2010 ◽  
Vol 50 (6) ◽  
pp. 1196-1202 ◽  
Author(s):  
Frederick A. Matheu ◽  
Steve J. McFaul
Keyword(s):  
Platelet Aggregation ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Inhibit Platelet Aggregation

The Effect of Anaesthetic Agents on Platelet Function

1991 ◽  
Vol 19 (4) ◽  
pp. 495-505 ◽  
Author(s):  
N. M. Gibbs
Keyword(s):  
Platelet Aggregation ◽  
Platelet Function ◽  
Local Anaesthetic ◽  
Peak Plasma ◽  
Plasma Concentrations ◽  
Muscle Relaxants ◽  
Current Evidence ◽  
Inhibit Platelet Aggregation ◽  
Anaesthetic Agents ◽  
Thrombotic Complications

This paper reviews studies which have investigated the effect of anaesthetic agents on platelet function The results of these studies suggest that halothane is the only agent in current use which inhibits platelet function in concentrations used clinically. Nitrous oxide appears to cause only a modest inhibition, while enflurane and isoflurane appear to have minimal or negligible effects. There is no current evidence that intravenous induction agents opiates, or muscle relaxants affect platelet function. Reports indicate that local anaesthetic agents inhibit platelet aggregation, but only at concentrations far greater than peak plasma concentrations found during clinical use. Epidural anaesthesia may be associated with a reduction in platelet aggregation through a mechanism unrelated to direct local anaesthetic inhibition. The clinical significance of the effect of halothane on platelet function is not known. However, it is possible that halothane may affect bleeding or thrombotic complications in a similar manner to other ‘anti-platelet’ drugs.

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