Study of platelet aggregation induced by platelet activating factor (PAF) after administration of ticlopidine or aspirin.
Platelet aggregation induced by platelet activating factor (PAF) was studied in 95 subjects: 39 controls, 23 patients receiving aspirin and 33 receiving ticlopidine. Potentiation of aggregation by concentrations of adrenaline unable to induce aggregation when used alone was also assessed. The 33 patients treated with ticlopidine showed a highly significant fall of platelet aggregation (p less than 0.001) at the three concentrations of PAF used. The 23 subjects receiving aspirin showed a diminution of platelet aggregation induced by PAF due to inhibition of ADP release. In these last two groups, adrenaline often potentiated platelet aggregation. However, this phenomenon was absent in subjects having taken aspirin in the hours before blood was drawn. This study demonstrates ticlopidine's inhibitory action on PAF-induced aggregation and confirms ticlopidine's role in reducing platelet aggregation by ADP, which has previously been demonstrated.
D000328:Adult; D000368:Aged; D000925:Anticoagulants / Q000494:pharmacology*; D001241:Aspirin / Q000494:pharmacology*; D004837:Epinephrine / Q000494:pharmacology; D006801:Humans; D066298:In Vitro Techniques; D008875:Middle Aged; D010972:Platelet Activating Factor / Q000494:pharmacology*; D010974:Platelet Aggregation / Q000187:drug effects*; D013876:Thiophenes / Q000494:pharmacology*; D013988:Ticlopidine
D000925:Anticoagulants; D010972:Platelet Activating Factor; D013876:Thiophenes; D013988:Ticlopidine; D001241:Aspirin; D004837:Epinephrine