[Comparative study of platelet anti-aggregation effect of several anti-inflammatory agents]

The relationships between inflammation and platelets, particularly between inflammation and platelet aggregation, have been elucidated during the last two years. Platelet aggregation is greatly enhanced by PGE2 and PGF2 alpha prostaglandins, which act as mediators of inflammation through the part they play in the regulation of platelet cyclic AMP whose intracellular concentration is determined by PGE1. Recently, acetylsalicylic acid and indomethacin have been shown to inhibit the synthesis and release of PGE2 as well as platelet aggregation. These findings prompted the present study of the inhibitory effect on platelet aggregation of two antiinflammatory drugs, metiazinic acid and ketoprofen. Indomethacin was elected as the reference drug. Both agents studied inhibit platelet aggregation more strongly than indomethacin. Inhibition of the release reaction is significantly stronger with ketoprofen than with the reference drug. The authors believe that this in vitro trial, in which platelet aggregation is induced by collagen, is of special significance as it involves the same biologic phenomena as those which occur in vivo.