Aspirin fails to prevent experimental arterial thrombosis induced by oxygen free radicals

Oxygen free radicals generated in the lumen of a vessel seem to play a central role in myocardial reperfusion injury such as the no-reflow phenomenon (11). Platelet activation may be involved in this abnormality (19), so an antiplatelet therapy should be beneficial. Investigation in patients with severe ischemic symptoms had shown that heparin was more effective than aspirin in relieving pain and preventing acute myocardial infarction (16). But, aspirin remains a reference antithrombotic drug, acting by irreversibly acetylating cyclooxygenase in platelets and endothelial cells (14). Its potency to specifically protect against thrombosis associated with free radicals is reported in this study, by using a new experimental model where thrombosis is induced by anion superoxide and singlet oxygen generated by photoactivated rose bengal (10). The aim of this study was to test these two antithrombotic substances : heparin and aspirin in an experimental model of arterial thrombosis induced by generation of free radicals.