Why the study?
Does clopidogrel affect platelet activation, prostanoid and NO production, and platelet-subendothelium interaction differently than ticlopidine and aspirin in vitro?
Does clopidogrel affect platelet activation, prostanoid and NO production, and platelet-subendothelium interaction differently than ticlopidine and aspirin in vitro?
This in vitro study demonstrates that clopidogrel has potent antiplatelet effects via collagen pathways and favorable effects on NO and prostacyclin production compared to aspirin.
Answers are grounded in this paper and cite their sources.
Preclinical data should not guide antiplatelet choice; leaves open whether clopidogrel's in vitro advantages on NO and aggregation translate clinically.
Clopidogrel is an antiplatelet drug that belongs to the group of thienopyridines. Because of its main mechanism of action most studies of clopidogrel have centered on the platelet ADP pathway. The aim of the present study was to compare the effects of clopidogrel, ticlopidine, and aspirin, on platelet activation by collagen (the main inducer of platelet activation in vivo), prostanoid, and NO production, and the effects on blood perfusion experiments. Clopidogrel inhibited platelet aggregation induced in whole blood by collagen and TxB2 production to a greater extent than did ticlopidine. Prostacyclin synthesis did not change after incubation with thienopyridines, whereas aspirin inhibited synthesis in a dose-dependent manner. Thienopyridines increased NO production to a greater extent than did aspirin. All three drugs impaired the platelet-subendothelium interaction under flow conditions. With thienopyridines, the presence of endothelium did not modify the percentage of the surface coated by platelets.
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Arrebola et al. (2003) studied this question.
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