[Clinical-experimental studies on the inhibition of thrombocyte function with acetylsalicylic acid and with indobufen].
The mode of action of two inhibitors of platelet function is reported. At low doses both substances inhibit platelet aggregation, at higher doses they inhibit the availability of platelet factor 3 and liberation of platelet factor 4. Acetylsalicylic acid, however, possesses a long-lasting effect produced by irreversible acetylation of platelet membrane. This was demonstrated in a series of clinico-experimental studies in which 14C-labelled ASA was used. Indobufen was found to cause transitory changes of platelet function. It is easily washed out from platelets and binds loosely to cytosol proteins of platelets, as shown in studies with 14-C-labelled indobufen. In contrast to ASA, it exerts an effect on platelets lasting for a few hours only.
D001241:Aspirin / Q000494:pharmacology*; D006801:Humans; D007211:Indoles / Q000494:pharmacology; D054833:Isoindoles; D010654:Phenylbutyrates / Q000494:pharmacology; D010974:Platelet Aggregation / Q000187:drug effects*; D010977:Platelet Factor 3 / Q000032:analysis; D010978:Platelet Factor 4 / Q000032:analysis
D007211:Indoles; D054833:Isoindoles; D010654:Phenylbutyrates; D010977:Platelet Factor 3; D010978:Platelet Factor 4; C020371:indobufen; D001241:Aspirin
Klinisch-experimentelle Studien zur Hemmung der Thrombozytenfunktion mit Azetylsalizylsäure und mit Indobufen.