B.-N. MARINCU, MONICA NEAGU, OANA MUNTEANU, A. NEAGU
Department of Biophysics and Medical Informatics, Center for Modeling Biological Systems and Data Analysis, “Victor Babeş” University of Medicine and Pharmaceutics, Timişoara, 2, Piaţa Eftimie Murgu, 300041 Timişoara, Romania
Abstract. Platelet aggregation is important to stop bleeding. In certain pathologies, however, excessive platelet aggregation leads to atherothrombosis and ischemic events. The potentially lethal consequences of impaired platelet aggregation, explain the importance of quantitative studies of platelet function. Several techniques have been developed to measure the time course of in vitro platelet aggregation induced by agonsits such as ADP, epinephrine, collagen, arachidonic acid and ristocetin. Kinetic methods allow for a quantitative analysis of the time-dependence of the aggregation response, and point out the relative importance of the underlying processes. To describe ADP-induced platelet aggregation, we propose a kinetic model that includes three compartments: single platelets, aggregated platelets and deaggregated platelets (i.e. single platelets that have left an aggregate). We assume that deaggregated platelets have different adhesive properties than single platelets that have not been part of an aggregate. Our model is simpler than earlier models, and it is in accord with data obtained by light transmission aggregometry. Applied for healthy subjects and for patients with myeloproliferative disorders (MPD), our kinetic approach suggests that the rate of reaggregation is significantly reduced in MPD.
Key words: light transmission aggregometry, compartmental model, deaggregation, reaggregation, myeloproliferative disorders.
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