The effects of mefenamic acid on in vitro platelet functions, namely thrombininduced production of thiobarbituric acid-reactive substances (TBARS) and ADP-induced platelet aggregation, were investigated and compared with those of aspirin and flurbiprofen.
Mefenamic acid inhibited platelet TBARS production almost comparatively to aspirin and flurbiprofen. The inhibitory effects of these three drugs on platelets from patients with atherosclerotic vascular diseases were smaller than the effects on platelet from normal subjects. Percent inhibition, by mefenamic acid, on platelet TBARS production correlated positively with maximal aggregation in these subjects.
Mefenamic acid also strongly suppressed platelet aggregation. In contrast to aspirin and flurbiprofen, of which effects were limited solely on secondary aggregation, mefenamic acid abolished primary aggergation, as well. Therefore, besides being a strong inhibitor of platelet thromboxane generation, mefenamic acid may exert its anti-platelet action through unknown mechanism (s). Antiplatelet action of this drug can be also characterized by the result suggesting that the inhibition tends to be large on platelets with higher aggregatory activity.
