The Effect of Heparin on the Interaction of Factor VIII and Human Platelets &lt;i&gt;in vitro&lt;/i&gt;

Marco, Luigi De; Fabris, Fabrizio; Molaro, G; Girolami, Antonio

doi:10.1159/000214176

Pathophysiol Haemos Thromb

1977

DOI: 10.1159/000214176

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The Effect of Heparin on the Interaction of Factor VIII and Human Platelets <i>in vitro</i>

Luigi De Marco

Fabrizio Fabris

G Molaro

et al.

Abstract: Heparin was found to inhibit the interaction between human factor VIII and platelets. This was noted in two different systems, namely, platelet aggregation induced by neuraminidase-treated human cryoprecipitate and platelet aggregation induced by ristocetin-human factor VIII complex. Heparin appeared to have an inhibitory effect on the above systems similar to that reported on bovine factor VIII-induced platelet aggregation.

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Cited by 4 publications

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“…The aggregation was calculated as a variation of optic density between the PRP and PPP (Girolami et nl. 1975, De Marco et al 1977.…”

mentioning

confidence: 99%

Effect of heparin on in vivo platelet factor 4 (PF4) release and platelet aggregation after aspirin administration

Cella

Menardo

Girolami

1980

Clinical &Amp; Laboratory Haematology

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SurnrnuryWe studied the release in vivo of platelet specific proteins platelet factor 4 (PF4) and /l-thromboglobulin (PTG), and confirmed that only PF4 is released, after heparin intravenous administration. A good correlation was found between platelet count and PF4 and this seems at variance with the idea that the source of released PF4 is vascular endothelium rather than platelets; however, such a possibility cannot be excluded. Although platelet function was blocked by aspirin injection heparin was still able to induce the release of PF4 and exerted a potentiating effect on platelet aggregation induced by ADP and collagen.

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“…The aggregation was calculated as a variation of optic density between the PRP and PPP (Girolami et nl. 1975, De Marco et al 1977.…”

mentioning

confidence: 99%

Effect of heparin on in vivo platelet factor 4 (PF4) release and platelet aggregation after aspirin administration

Cella

Menardo

Girolami

1980

Clinical &Amp; Laboratory Haematology

Self Cite

View full text Add to dashboard Cite

show abstract

Normal and low molecular weight heparins: interaction with human platelets

Fabris

Fussi

Casonato

et al. 1983

Eur J Clin Investigation

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Porcine mucosal heparin was chemically depolymerized. The depolymerization was stopped at different steps to obtain two low molecular weight (LMW) heparins with a molecular weight of 10 000 and 6000, respectively. The LMW heparins were tested in vitro for anti-clotting activities and for platelet serotonin release in different systems in comparison with normal heparins, dermatan and heparan sulphate. After addition of various amounts of heparin preparations to washed platelets, no significant release was observed for all tested heparins. On the contrary, different heparins showed an inhibition of serotonin-release induced by collagen in platelet rich plasma, whereas the ADP-induced release was increased. The effect on the platelet release appears related to the molecular weight. In fact, it is significant only for normal heparins whereas it is not for LMW heparins. A good relation was observed, also, between anti-activated factor X activity/antiglobal clotting activity (Xa/APTT) ratio of different heparins and the effect on platelet release.

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Distribution of plasma fibronectin (cold-insoluble globulin) and components of the factor VIII complex after heparin-induced precipitation of plasma

Amrani¹,

Mosesson²,

Hoyer³

1982

Blood

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Factor VIII procoagulant (VIII:C) activity, factor VIII coagulant antigen (VIII:CAg), von Willebrand ristocetin cofactor (VIIIR:RC) activity, factor VIII-related antigen (VIIIR:Ag), and plasma fibronectin (CIg; cold-insoluble globulin) were measured in the heparin precipitable fraction (HPF) and heparin supernatant fraction (HS) of normal human plasma. Following heparin induced precipitation, most measurable VIII:C activity (77% +/- 24%) was recovered in the HS. Although there was little VIII:C activity (less than 1%) in the HPF, 20% +/- 6.5% VIII:CAg was present as well as CIg (81% +/- 5.6%). VIIIR:RC activity (72% +/- 12%), and VIIIR:Ag (34 +/- 5.2%). As assessed by Na dodecyl SO4 glyoxyl agarose electrophoresis, the multimeric forms of plasma VIIIR:Ag could be resolved into a series of bands. Larger multimers tended to precipitate with the HPF whereas the smaller multimers tended to remain supernatant. Plasma from a subject with congenital afibrinogenemia was also studied. Although the afibrinogenemic HPF contained CIg, neither VIIIR:RC activity nor VIIIR:Ag was precipitated. However, both were present in the HPF from afibrinogenemic plasma to which fibrinogen had been added, suggesting that they are incorporated in this precipitate because of an affinity for fibrinogen. The ability of heparin to induce precipitation of CIg while leaving most VIII:C activity in the supernatant plasma may be useful in the preparation of procoagulant-rich plasma subfractions, since VIII:C can subsequently be recovered in good yield by cryoprecipitation.

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The Effect of Heparin on the Interaction of Factor VIII and Human Platelets <i>in vitro</i>

Cited by 4 publications

References 15 publications

Effect of heparin on in vivo platelet factor 4 (PF4) release and platelet aggregation after aspirin administration

Effect of heparin on in vivo platelet factor 4 (PF4) release and platelet aggregation after aspirin administration

Normal and low molecular weight heparins: interaction with human platelets

Distribution of plasma fibronectin (cold-insoluble globulin) and components of the factor VIII complex after heparin-induced precipitation of plasma

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