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Updated: Jul 24, 2026
Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation
Published on: April 6, 2017
[Studies of platelet aggregation in six cases of EDTA-dependent pseudothrombocytopenia]
1Department of Internal Medicine, Himeji National Hospital.
Peripheral blood count was performed by a Coulter Model S Plus STKR on six pseudothrombocytopenia patients (age: 16-70, 2 men and 4 women) using three different anticoagulants. Treatment with ethylene diamine tetraacetate (EDTA, 1 mg/ml) or sodium heparin (25 U/ml) aggregated platelets, but sodium citrate (3.8%, 1:9) had no effect. Smear examination revealed much platelet clumping but the satellite phenomenon was not present. No specific pattern was elucidated concerning cell size distribution curves between treatment by EDTA and heparin. Theophylline (10 mg/ml) and prostaglandin I2 (1 microM) inhibited EDTA-induced platelet aggregation but aspirin (1.8 mM) did not. On the other hand, these three substances inhibited heparin-induced platelet aggregation. These findings, taken together, suggested that EDTA and heparin initiated platelet activation and EDTA-induced platelet aggregation might be a process unrelated to thromboxane A2 production. Heparin may not be a suitable anticoagulant since it aggregates platelets of some healthy individuals.
Peripheral blood count was performed by a Coulter Model S Plus STKR on six pseudothrombocytopenia patients (age: 16-70, 2 men and 4 women) using three different anticoagulants. Treatment with ethylene diamine tetraacetate (EDTA, 1 mg/ml) or sodium heparin (25 U/ml) aggregated platelets, but sodium citrate (3.8%, 1:9) had no effect. Smear examination revealed much platelet clumping but the satellite phenomenon was not present. No specific pattern was elucidated concerning cell size distribution curves between treatment by EDTA and heparin. Theophylline (10 mg/ml) and prostaglandin I2 (1 microM) inhibited EDTA-induced platelet aggregation but aspirin (1.8 mM) did not. On the other hand, these three substances inhibited heparin-induced platelet aggregation. These findings, taken together, suggested that EDTA and heparin initiated platelet activation and EDTA-induced platelet aggregation might be a process unrelated to thromboxane A2 production. Heparin may not be a suitable anticoagulant since it aggregates platelets of some healthy individuals.
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