Low dose aspirin does not prevent fibrinolytic response to venous occlusion.

Interest in the antithrombotic potential of low-dose aspirin is based on its ability to inhibit thromboxane (Tx)A2-related platelet function with concomitant sparing of vascular prostacyclin (PGI2) production. The aim of this study was to investigate the effect of low-dose aspirin (20 mg daily for 7 days) on the increase in fibrinolytic activity in healthy volunteers after venous occlusion. We also tested the effect of high-dose aspirin (650 mg X 2), of salicylate (569 mg X 2) and of indobufen (200 mg X 2), a new cyclo-oxygenase inhibitor unrelated to salicylates. Low-dose aspirin reduced serum TxB2 generation by about 90% and suppressed arachidonate-induced platelet aggregation. In contrast, fibrinolytic activity, measured by the euglobulin lysis area and the euglobulin lysis time, was not significantly affected. Both high-dose aspirin and indobufen significantly inhibited TxB2 generation and the rise in fibrinolytic activity induced by venous occlusion, without affecting the pre-occlusion values. Salicylate did not significantly affect any parameter studied. Besides offering a favorable solution to the "aspirin dilemma" related to the TxA2/PGI2 balance, low-dose aspirin might leave intact the fibrinolytic capacity of the vessel wall.