Abstract
Addition of arachidonic acid (0.1 mM) to a washed platelet suspension obtained from guinea pigs resulted in platelet aggregation and formation of malonyldialdehyde in vitro. These were inhibited by 2-(5H-[1] benzopyrano [2, 3-b] pyridin-7-yl) propionic acid (pranoprofen), indomethacin and acetylsalicylic acid. The concentrations causing a 50% inhibition of malonyldialdehyde formation were 0.35 μM for indomethacin, 4.6 μM for pranoprofen, and 77 μM for acetylsalicylic acid. Oral treatment of guinea pigs with pranoprofen (0.01 mg/kg), indomethacin (1 mg/kg), or acetylsalicylic acid (10 mg/kg) resulted in inhibition of platelet aggregation induced by the addition of arachidonic acid (0.1 mM). The increased pulmonary pressure with a concomitant decrease of platelet counts induced by the intravenous injection of arachidonic acid (400 μg/kg) to guinea pigs was inhibited by oral treatment with the above agents. These results suggest that pranoprofen inhibits the platelet aggregation by affecting the pathway concerned with prostaglandin synthesis, and may have an antithrombotic activity.
