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.
D015121:6-Ketoprostaglandin F1 alpha / Q000097:blood; D000704:Analysis of Variance; D001241:Aspirin / Q000008:administration & dosage* / Q000627:therapeutic use; D005342:Fibrinolysis / Q000187:drug effects*; D006400:Hematocrit; D006801:Humans; D054833:Isoindoles; D010654:Phenylbutyrates / Q000008:administration & dosage / Q000627:therapeutic use; D013927:Thrombosis / Q000188:drug therapy*; D013929:Thromboxane B2 / Q000097:blood
D054833:Isoindoles; D010654:Phenylbutyrates; D013929:Thromboxane B2; D015121:6-Ketoprostaglandin F1 alpha; C020371:indobufen; D001241:Aspirin