Thromb Haemost 2006; 96(06): 781-788
DOI: 10.1160/TH06-05-0242
Platelets and Blood Cells
Schattauer GmbH

Multiple electrode aggregometry: A new device to measure platelet aggregation in whole blood

Orsolya Tóth
1   Institute for Prevention of Cardiovascular Diseases, University of Munich, Munich, Germany
2   1stDepartment of Medicine, University of Pécs, Pécs, Hungary
Andreas Calatzis
3   Department of Transfusion Medicine and Hemostaseology, University of Munich, Munich, Germany
Sandra Penz
1   Institute for Prevention of Cardiovascular Diseases, University of Munich, Munich, Germany
Hajna Losonczy
2   1stDepartment of Medicine, University of Pécs, Pécs, Hungary
Wolfgang Siess
1   Institute for Prevention of Cardiovascular Diseases, University of Munich, Munich, Germany
› Author Affiliations
Financial support: The study was supported by the August-Lenz foundation (O.T.) and the graduate program GK438 “Vascular Biology in Medicine” Deutsche Forschungsgemeinschaft (S.P.; W.S).
Further Information

Publication History

Received 05 May 2006

Accepted after resubmission 09 October 2006

Publication Date:
29 November 2017 (online)


Several methods are used to analyse platelet function in whole blood. A new device to measure whole blood platelet aggregation has been developed, called multiple electrode platelet aggregometry (MEA). Our aim was to evaluate MEA in comparison with the single platelet counting (SPC) method for the measurement of platelet aggregation and platelet inhibition by aspirin or apyrase in diluted whole blood. Platelet aggregation induced by different concentrations of ADP, collagen and TRAP-6 and platelet inhibition by apyrase or aspirin were determined in citrateor hirudin-anticoagulated blood by MEA and SPC. MEA indicated that spontaneous platelet aggregation was lower, and stimulated platelet aggregation was higher in hirudin- than citrate-anticoagulated blood. In hirudin-anticoagulated, but not citrate-anticoagulated blood, spontaneous platelet aggregation measured by MEA was inhibited by apyrase. For MEA compared with SPC the dose response-curves of agonist-induced platelet aggregation in citrate- and hirudin-blood showed similar EC50 values for TRAP, and higher EC50 values for ADP (non-significant) and collagen (p<0.05). MEA and the SPC method gave similar results concerning platelet-inhibition by apyrase and aspirin. MEA was more sensitive than SPC to the inhibitory effect of aspirin in collagen-induced aggregation. In conclusion, MEA is an easy, reproducible and sensitive method for measuring spontaneous and stimulated platelet aggregation, and evaluating antiplatelet drugs in diluted whole blood. The use of hirudin as an anticoagulant is preferable to the use of citrate. MEA is a promising technique for experimental and clinical applications.

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