Platelet Aggregate Formation in Peripheral Blood Anti-coagulated with Sodium Heparin is Facilitated by Mixing

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  • ヘパリン採血における混和による血小板凝集

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Peripheral blood anti-coagulated with sodium heparin (25U/ml) form 60 healthy volunteers invariably had a reduced platelet count, when whole blood was mixed in the presence of air. Smear findings similar to those observed in EDTA-induced pseudothrombocytopenia and the counteracting effect of prostaglandin E1 (1μM) on thrombocytopenia suggest that this thrombocytopenia is due to platelet activation and aggregate formation. Mixing may activate platelets, because the extent of thrombocytopenia had a positive correlation with the air volume and mixing intensity. Aspirin (1.8mM) and 5-HT2 blocker (sarpogrelate 100μM) also inhibited this phenomenon. These findings suggest that the mechanism of platelet activation might be partly related to arachidonate metabolism and serotonin release. Oxygen appears to have no direct effects. It is suggested that red blood cells and/or white blood cells participate in platelet activation, because platelet aggregation of platelet-rich plasma was less than that of whole blood. 5-lipoxygenase inhibitor had little effect. To measure platelet counts, it appears essential to eliminate the copresence of air in blood samples anti-coagulated with heparin.

Journal

  • Rinsho Ketsueki

    Rinsho Ketsueki 38 (4), 323-330, 1997

    The Japanese Society of Hematology

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