title: Multiple electrode aggregometry: a new device to measure platelet aggregation in whole blood.
abstract: 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.
authors.affiliation: Institute for Prevention of Cardiovascular Diseases, University of Munich, Munich, Germany. orsolya.toth@aok.pte.hu
authors.forename: Orsolya
authors.initials: O
authors.lastname: Tóth
authors.forename: Andreas
authors.initials: A
authors.lastname: Calatzis
authors.forename: Sandra
authors.initials: S
authors.lastname: Penz
authors.forename: Hajna
authors.initials: H
authors.lastname: Losonczy
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Siess
mesh_terms: D000244:Adenosine Diphosphate / Q000494:pharmacology; D000925:Anticoagulants / Q000494:pharmacology; D001081:Apyrase / Q000494:pharmacology; D001241:Aspirin / Q000494:pharmacology; D001793:Blood Preservation / Q000379:methods; D002951:Citrates / Q000494:pharmacology; D003094:Collagen / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D017097:Electric Impedance; D004566:Electrodes; D006629:Hirudins / Q000494:pharmacology; D006801:Humans; D066298:In Vitro Techniques; D010446:Peptide Fragments / Q000494:pharmacology; D010974:Platelet Aggregation / Q000187:drug effects; D010975:Platelet Aggregation Inhibitors / Q000494:pharmacology; D010976:Platelet Count; D010979:Platelet Function Tests / Q000295:instrumentation*; D012016:Reference Values; D015203:Reproducibility of Results; D012680:Sensitivity and Specificity; D000077559:Sodium Citrate; D013997:Time Factors
chemical_list: D000925:Anticoagulants; D002951:Citrates; D006629:Hirudins; D010446:Peptide Fragments; D010975:Platelet Aggregation Inhibitors; C082835:thrombin receptor peptide (42-47); D000077559:Sodium Citrate; D000244:Adenosine Diphosphate; D003094:Collagen; D001081:Apyrase; D001241:Aspirin