Aspirin inhibits platelet function independent of the acetylation of cyclo-oxygenase.

Aspirin inhibits platelet function and prevents thrombosis in some clinical situations. This antithrombotic effect is attributed to the irreversible inhibition of platelet thromboxane A2 synthesis, an effect which is achieved by a low dose of aspirin. There is some evidence that higher doses of aspirin may have additional antithrombotic effects. To test this possibility, we measured the effect of high and low dose aspirin on hemostasis in vivo and platelet function ex vivo in the rabbit. Both carotid arteries were isolated. One was replaced with a 2 cm piece of polyethylene tubing and the other was left intact. The prosthetic and intact vessels were then punctured with a needle and the time take for bleeding from each to cease was measured. Aspirin (3 and 100 mg/kg given 1 or 20 hours before hand) had no effect on the bleeding from the intact vessel, but prolonged the bleeding time in the prosthetic vessel in a dose-related manner. Washed platelets obtained from the 100 mg/kg-treated rabbits were less responsive to collagen and thrombin than platelets obtained from the 3 mg/kg-treated rabbits which in turn, were less responsive than control platelets. This additional effect of aspirin on platelet function was not due to the further inhibition of platelet thromboxane A2 release nor to further inhibition of the platelet release phenomenon. It is suggested that the enhanced effect of high dose aspirin on haemostasis from the arterial prosthesis is related to the second platelet inhibiting effect of aspirin.