Concerning anticoagulation:
A. Heparin decreases the efficacy of antithrombin IIIHeparin activates antithrombin III. The intrinsic and extrinsic coagulation pathways converge at Factor X. The antithrombotic effect of dextran is mediated through its binding of erythrocytes, platelets, and vascular endothelium, increasing their electronegativity and thus reducing erythrocyte aggregation and platelet adhesiveness. Dextrans also reduce Factor VIII-Ag von Willebrand Factor, thereby decreasing platelet function. Low-dose, long-term aspirin use irreversibly blocks the formation of thromboxane A2 in platelets, producing an inhibitory effect on platelet aggregation. Aspirin inhibits collageninduced platelet aggregation and ADP-induced platelet aggregation, as well as blocking the release of ADP from platelets. ADP is known to be a potent platelet-aggregating substance. Aspirin acts on cyclo-oxygenase by causing irreversible acetylation of the enzyme, and therefore the effect is irreversible for the life of that platelet (7-10 days). Other non-steroidal antiinflammatory analgesics have a reversible action on that enzyme, and hence only act until the drug is cleared from the circulation.