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March - Anti-platelet drugs mechanism
Blood platelets are activated by collagen released at the site of a vascular injury, by the change of blood flow (shear stress) and by thrombin formation. Platelets also increase their own activation by two mechanisms: the release of ADP and the thromboxane A2generation (TXA2), a potent platelet agonist. These mechanisms are also anti-platelet drugs’ main pharmacological targets: ADP receptor antagonists (thienopyridines) blockplatelet ADP receptors (P2Y12). Aspirin blocks cyclooxygenase (COX1), responsible for generating thromboxane A2 (TXA2). Sysmex’s CS-series coagulation analysers (exceptCS-1600) monitor anti-platelet drugs by Revohem reagents (ADP, arachidonic acid).
