Inhibition of smoking-induced platelet aggregation by aspirin and pycnogenol

The effects of a bioflavonoid mixture, Pycnogenol, were assessed on platele t function in humans. Cigarette smoking increased heart rate and blood pres sure. These increases were not influenced by oral consumption of Pycnogenol or Aspirin just before smoking. However, increased platelet reactivity yie lding aggregation 2 hours after smoking was prevented by 500 mg Aspirin or 100 mg Pycnogenol in 22 German heavy smokers. In a group of 16 American smo kers, blood pressure increased after smoking. It was unchanged after intake of 500 mg Aspirin or 125 mg Pycnogenol. In another group of 19 American sm okers, increased platelet aggregation was more significantly reduced by 200 than either 150 mg or 100 mg Pycnogenol supplementation. This study showed that a single, high dose, 200 mg Pycnogenol, remained effective for over 6 days against smoking-induced platelet aggregation. Smoking increased plate let aggregation that was prevented after administration of 500 mg Aspirin a nd 125 mg Pycnogenol. Thus, smoking-induced enhanced platelet aggregation w as inhibited by 500 mg Aspirin as well as by a lower range of 100-125 mg Py cnogenol. Aspirin significantly (p<0.001) in creased bleeding time from 167 to 236 seconds while Pycnogenol did not. These observations suggest an adv antageous risk-benefit ratio for Pycnogenol. (C) 1999 Elsevier Science Ltd. All rights reserved.