Abstract
The present study investigates the effects of aspirin (100 mg every second day for 14 days) on platelet function in nine healthy non-smokers and in nine healthy habitual smokers. There was a significantly (P<0.05) stronger inhibition of collagen (0.6 mu g/ml)- and ADP (2 mu M)-induced platelet aggregation by aspirin in smokers as compared to non-smokers. This difference occurred in the presence of an almost complete (>95%) inhibition of thromboxane A 2 (TXA 2 ) synthesis in both groups. The platelet capacity to generate TXA 2 in vitro was significantly reduced in smokers, urinary excretion of TXA 2 , however, was significantly increased. Thus, the better susceptibility of smokers to anti-aggregatory effects of aspirin is very likely to be related to a chronic smoking-induced alteration of platelet TXA 2 system. Cessation of smoking should, therefore, be encouraged.