[Thrombocyte function of healthy probands taking 50 mg of acetylsalicylic acid per day]

The antithrombotic effect of acetylsalicylic acid (ASS) is attributed in part to its inhibitory action on platelet cyclooxygenase and, thereby, thromboxane A2 (TXA2) formation. The therapeutic goal of low-dose ASS regimens was the development of a preparation showing a high inhibitory capacity on platelet TXA2 generation whilst leaving vascular prostaglandin I2 (PGI2) synthesis unaffected, thereby minimizing side effects. The effect of a new acid-resistant preparation of 50 mg ASS (Thrombo-ASS 50 mg) on plasma levels of ASS, salicylate, TXB2, 11-dehydro-thromboxane B2, serum thromboxane B2 and malonyl dialdehyde, the conversion of exogenous 14C-arachidonic acid to TXB2 and hydroxy-5,8,10-heptadecatrienoic acid (HHT), as well as on the urinary metabolites 2,3-dinor-6-oxo-PGF1 alpha and 2,3-dinor TXB2, were compared in a crossover trial to those of a marketed preparation (Aspirin 100 mg) in healthy volunteers after a single dose and repeated administration of ASS. While platelet activity was inhibited by both the test and the reference substance to a comparable extent, vascular PGI2 production (as determined by urinary 2,3-dinor-6-oxo-PGF1 alpha excretion) was less affected by the test substance. These findings confirm the claim that a dosage of 50 mg ASS administered daily as an enteric coated or uncoated tablet is sufficient to almost completely block platelet cyclooxygenase, while the respective vascular enzyme is only minimally affected.