Inhibition by ticlopidine of Paf-acether-induced in vitro aggregation of rabbit and human platelets.
Ticlopidine was incubated in vitro with rabbit or human washed platelets and aggregations were triggered by submaximal concentrations of adenosine-5'-diphosphate (ADP), arachidonic acid (AA) and Paf-acether (platelet-activating factor), the mediators of the three known pathways of platelet activation. Inhibition of Paf-acether-induced rabbit platelet aggregation was proportional to the concentrations of Ticlopidine used. The same range of inhibition by Ticlopidine was observed when aggregations were triggered by the two other agonists. Human platelet aggregation induced by Paf-acether was also inhibited by Ticlopidine. Inhibition was increased when platelets were rendered insensitive to ADP and AA. Our results show that Ticlopidine inhibits human and rabbit platelet aggregation triggered by Paf-acether through a mechanism not related to the inhibition of the ADP and prostaglandin pathways.
D000244:Adenosine Diphosphate / Q000494:pharmacology; D000818:Animals; D001095:Arachidonic Acids / Q000494:pharmacology; D006801:Humans; D010972:Platelet Activating Factor / Q000037:antagonists & inhibitors / Q000502:physiology*; D010974:Platelet Aggregation / Q000187:drug effects*; D011817:Rabbits; D013876:Thiophenes / Q000494:pharmacology*; D013988:Ticlopidine
D001095:Arachidonic Acids; D010972:Platelet Activating Factor; D013876:Thiophenes; D000244:Adenosine Diphosphate; D013988:Ticlopidine