Our studies on the urinary excretion of 2,3-dinor-TxB2 and 2,3-dinor-6-keto-PGF1 alpha in humans strongly indicate that these metabolites are good indicators of the in vivo synthesis of TxA2 and PGI2. Our finding that physical exercise increases PGI2 synthesis was of particular importance for the design of adequate studies on the effects of various drugs on the in vivo formation of PGI2. The rapid recovery (within 3-4 h) of PGI2 formation found following administration of 1.0 g of aspirin together with the long-lasting inhibition of TxA2, suggests that in the prophylaxis of thromboembolic events an intermittent dosage of 0.5 g of aspirin every third day should be a better alternative than daily low or high doses of aspirin. The increased TxA2 formation found in patients with acute myocardial infarction, deep vein thrombosis and in patients following insertion of synthetic surfaces into the circulation, is very likely a reflection of an increased activation of platelets. The increased TxA2 synthesis may cause further platelet activation, vasoconstriction and activation of the coagulation system. Thus, theoretically, inhibition of TxA2 could diminish platelet activation and reduce the risk of thrombotic complications. It is well known that the interaction between platelets and the vessel wall plays an important role in haemostasis and in the development of thrombosis. On the basis of its biological properties, PGI2 may play a local haemostatic role in the regulation of this interaction. Our studies of myocardial infarction and deep vein thrombosis clearly demonstrate the involvement of PGI2 in those diseases.(ABSTRACT TRUNCATED AT 250 WORDS)