Factor VIII-von Willebrand factor requires calcium for facilitation of platelet adherence

Sakariassen, Kjell S.; Ottenhof-Rovers, Mieke; Sixma, Jan J.

doi:10.1182/blood.v63.5.996.996

Cited by 70 publications

(9 citation statements)

References 25 publications

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“…Where there are differences there is a tendency for responses to be blunted in citrated blood compared with heparinized blood. This is most likely explained by citrateÕs calcium chelating action reducing the calcium available to the platelet, and so reducing calciumdependent responses, as has been previously demonstrated [9,15,20,21]. Citrate anticoagulation leads to an extracellular calcium concentration of around 50 lM, whereas non-chelating anticoagulation, by heparin for example, maintains an extracellular calcium level in the millimolar range [15,22].…”

Section: Discussionmentioning

confidence: 99%

Heparin but not citrate anticoagulation of blood preserves platelet function for prolonged periods

Truss

Armstrong

Liverani

et al. 2009

Journal of Thrombosis and Haemostasis

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To cite this article: Truss NJ, Armstrong PCJ, Liverani E, Vojnovic I, Warner TD. Heparin but not citrate anticoagulation of blood preserves platelet function for prolonged periods. J Thromb Haemost 2009; 7: 1897-905.Summary. Background: Current guidelines state that platelet aggregation studies should be conducted within 4 h of venepuncture because of the decline in sensitivity to platelet agonists. This constrains studies of platelet activity in clinical situations where samples need to be transported or there are unavoidable delays prior to assessment. Objectives: The aim of the present study was to compare systematically the responses of platelets stored in the presence of either citrate or heparin, the two most widely used anti-coagulants, using a range of standard techniques. Methods: Blood was taken from healthy volunteers and either assessed immediately or stored at ambient temperature (18-25°C) for 24 h. Platelet reactivity to a range of agonists was determined by a combination of 96-well plate techniques; light transmission aggregometry, thrombi adhesion, ATP and ADP release, and TxA 2 release; by whole blood aggregometry; and by PFA-100. Results and conclusions: Testing using 96-well plate techniques allowed for the simultaneous measurement of responses to multiple concentrations of multiple agonists. The responses of platelets from blood anticoagulated with heparin were predominantly preserved in all assays after 24 h storage, whereas, responses of platelets stored in blood anti-coagulated with citrate were greatly diminished. Consequently, anti-coagulation with heparin, but not citrate, preserves platelet responses for up to 24 h as determined by a range of techniques.

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Section: Discussionmentioning

confidence: 99%

Heparin but not citrate anticoagulation of blood preserves platelet function for prolonged periods

Truss

Armstrong

Liverani

et al. 2009

Journal of Thrombosis and Haemostasis

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“…However, the signals that modulate the coagulation of platelets and their de-aggregation remain unclear. Thrombus formation involves three functionally independent pathways that mediate the interactions between circulating blood cells and the cells of the vessel wall: eicosanoids (PGI 2 and TxA 2 ); biological gases (NO and CO); ectonucleotidase (CD39) ( 4 ) ; Ca ions ( 41 ) . Numerous reports have recognised that platelets play a pivotal role in arterial thrombus formation through TxA 2 and PGI 2 secretion ( 4 – 6 , 26 , 27 ) .…”

Section: Discussionmentioning

confidence: 99%

Modulation of platelet aggregation-related eicosanoid production by dietary F-fucoidan from brown algaLaminaria japonicain human subjects

et al. 2013

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Laminaria japonica is traditionally eaten in Japan as a beneficial food for thrombosis. The alga contains two specific ingredients, a xanthophyll fucoxanthin (FX) and a polysaccharide, F-fucoidan (FD). The aim of the present study was to investigate whether FX or FD exhibited anti-thrombotic effects. For this purpose, three types of capsules, containing 1 mg FX, 400 mg fucoidan, and both, were prepared from the alga and administered to volunteers for 5 weeks. The dose of FD or FD þ FX significantly shortened lysis time (LT) of the thrombus measured by a global thrombosis test in the blood, but FX did not. Examining the mechanism, dietary FD increased H 2 O 2 and the secretion of prostacyclin (PGI 2 ), a potent inhibitor of platelet aggregation, in the blood, although FD was under the detection limit in the blood, determining with its monoclonal antibody. Furthermore, in mouse experiments, dietary FD was totally excreted into the faeces and was not incorporated into the blood. We then employed a co-culture system of a Caco-2 cell monolayer with fresh human blood. The addition of FD to Caco-2 cells stimulated the expression of NADPH oxidase 1 (NOX1) and dual oxidase 2 (DUOX2) mRNA and secreted H 2 O 2 onto the blood side accompanied by a significant increase in serum PGI 2 production. These effects were invalidated by the combined addition of FD with its monoclonal antibody. The results suggested that dietary FD stimulated the expression of H 2 O 2 -producing enzymes in intestinal epithelial cells and released H 2 O 2 into the blood, which played a signalling role to increase PGI 2 production and then shortened LT for thrombi.

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“…Laboratory techniques. Blood collection, measurement of the bleeding time, haematocrit, platelet count, platelet volume and platelet aggregation studies were performed as described (Sakariassen et al, 1984a). FVIII-VWF was purified from human cryoprecipitate as indicated by Bolhuis et a1 (1 98 1).…”

Section: Methodsmentioning

confidence: 99%

“…A small perfusion chamber was used (Sakariassen et aI, 1984a), which has a distance between the outer chamber wall and the rod with mounted artery of 0.60 mm. Subendothelium of human umbilical arteries (Sakariassen et al, 1984a), which was produced by brief air exposure of the artery (Sakariassen et al, 1980), was exposed to recirculating perfusates for 3 min at wall shear rates of 1000 s-l and 2500 s-l corresponding to flow rates of 45 ml/min and 107 ml/min respectively. Prior to the perfusion runs, the artery segments were treated briefly with 0.1 M aspirin (A 53 76, Crystalline, Sigma, St Louis, Mo.)…”

Section: Methodsmentioning

confidence: 99%

“…Prior to the perfusion runs, the artery segments were treated briefly with 0.1 M aspirin (A 53 76, Crystalline, Sigma, St Louis, Mo.) as previously described (Sakariassen et al, 1984a) in order to inhibit prostacyclin production (Burch et al,19 78) which effects platelet interaction with the subendothelium (Weiss & Turitto,19 79). Platelet interaction with the subendothelium was quantified by morphometry (Baumgartner et al, 1976).…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Differentiation of patients with subtype IIb‐like von Willebrand's disease by means of perfusion experiments with reconstituted blood

Sakariassen¹,

Nieuwenhuis²,

Sixma³

1985

Br J Haematol

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Four unrelated patients with a bleeding diathesis (bleeding time longer than 30 min), some spontaneous platelet aggregation, thrombocytopenia and large platelets, had decreased levels of factor VIII-von Willebrand factor (FVIII-VWF) related properties and impaired platelet adherence to human artery subendothelium. The largest multimers of plasma FVIII-VWF were absent and enhanced ristocetin induced platelet aggregation in platelet-rich plasma was observed. 'Pseudo-von Willebrand's disease' was excluded, because FVIII-VWF from normal subjects did not initiate platelet aggregation. Perfusion studies with reconstituted blood, consisting of respectively patient platelets in normal plasma or normal platelets in patient plasma, yielded evidence for an intrinsic platelet abnormality in two out of the four patients and a plasma defect in the other two patients. Similar experiments with platelets and plasma from four patients with von Willebrand's disease (VWD) subtype I and four patients with VWD subtype IIa showed that the impaired platelet adherence in blood from these patients was caused by a plasma defect. These experiments indicate that patients with laboratory findings in many respects similar to those originally reported for patients with VWD subtype IIb may represent a heterogeneous group of individuals. The data derived from our study imply that perfusion experiments with reconstituted blood offer a new approach in characterization of these patients, which may be more relevant for the treatment of the patients than characterization by ristocetin induced adsorption of FVIII-VWF to platelets.

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Factor VIII-von Willebrand factor requires calcium for facilitation of platelet adherence

Cited by 70 publications

References 25 publications

Heparin but not citrate anticoagulation of blood preserves platelet function for prolonged periods

Heparin but not citrate anticoagulation of blood preserves platelet function for prolonged periods

Modulation of platelet aggregation-related eicosanoid production by dietary F-fucoidan from brown algaLaminaria japonicain human subjects

Differentiation of patients with subtype IIb‐like von Willebrand's disease by means of perfusion experiments with reconstituted blood

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