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https://hdl.handle.net/123456789/340| Τύπος: | Αναρτημένη ανακοίνωση (poster) |
| Τίτλος: | The effect of dabigatran and rivaroxaban on thrombin- and FXa-induced platelet aggregation |
| Συγγραφέας: | [EL] Παπαδάκη, Στυλιανή[EN] Papadaki, Styliani [EL] Μοσχονάς, Ηρακλής[EN] Moschonas, Iraklis [EL] Σιδηροπούλου, Σοφία[EN] Sidiropoulou, Sofia [EL] Τσελέπης, Αλέξανδρος[EN] Tselepis, Alexandros |
| Ημερομηνία: | Ιου-2019 |
| Περίληψη: | Background: Thrombin and FXa are the major serine proteases of the coagulation cascade, which also activate various cell types through protease-activated receptors (PARs). Dabigatran and rivaroxaban are direct oral anticoagulants (DOACs) that inhibit thrombin’s and FXa’s action, respectively, and are used in everyday clinical practice. Aim: We investigated the effect of dabigatran and rivaroxaban on thrombin- and FXa-induced platelet aggregation, respectively, in vitro. Methods: Whole blood from apparently healthy volunteers was collected and washed platelets were isolated and adjusted to 250,000 platelets/μl. Platelets were activated with various concentrations of thrombin or FXa to establish the concentration exhibiting the maximum effect. In subsequent experiments, washed platelets were incubated with various concentrations of dabigatran (1-10nM) and rivaroxaban (0.5-20nM) for 1min at 37oC before activation with thrombin or FXa, respectively. Platelet aggregation was monitored using light transmittance aggregometry, until the stabilization of the aggregation curve. Results: Thrombin induced platelet aggregation, which reached a maximum of 80-90% at 4min, at a dose of 0.1U/mL. FXa induced platelet aggregation, which reached a maximum of 80-90% at 20min, at a dose of 0.025nM. Dabigatran and rivaroxaban inhibited platelet aggregation induced by 0.1U/mL thrombin and 0.025nM FXa, in a dose-dependent manner, exhibiting IC50 values of 4.1nM and 3.5nM, respectively. Conclusions: Dabigatran and rivaroxaban strongly inhibit thrombin- and FXa-induced platelet aggregation, respectively. The above results suggest that through inhibition of platelet activation, these DOACs may prevent atherothrombotic events, in which platelets play a prominent role, in addition to their beneficial antithrombotic effects in venous thromboembolism. |
| Γλώσσα: | Αγγλικά |
| Τόπος δημοσίευσης: | Athens |
| Σελίδες: | 1 |
| Θεματική κατηγορία: | [EL] Άλλες Ιατρικές Επιστήμες[EN] Other Medical Sciences |
| Κάτοχος πνευματικών δικαιωμάτων: | © by the authors. |
| Όνομα εκδήλωσης: | 26th International Congress on Thrombosis (ICT) |
| Τοποθεσία εκδήλωσης: | Athens, Greece |
| Ημ/νία έναρξης εκδήλωσης: | 19/06/2019 |
| Ημ/νία λήξης εκδήλωσης: | 22/06/2019 |
| Σημειώσεις: | The present research has been co-financed by the Operational Program "Human Resources Development, Education and Lifelong Learning" and is co-financed by the European Union (European Social Fund) and Greek national funds. Congress webpage: https://www.thrombosiscongress.org/ |
| Εμφανίζεται στις συλλογές: | Ερευνητικές ομάδες |
Αρχεία σε αυτό το τεκμήριο:
| Αρχείο | Περιγραφή | Σελίδες | Μέγεθος | Μορφότυπος | Έκδοση | Άδεια | |
|---|---|---|---|---|---|---|---|
| Poster for EMLTD 2019.pdf | 271.48 kB | Adobe PDF | Δημοσιευμένη/του Εκδότη |  | Δείτε/ανοίξτε |