Platelet aggregation induced by ADP or epinephrine is enhanced in habitual smokers.

A novel system has been developed to evaluate biochemically induced platelet aggregation by means of a particle-counting technique that uses laser light scattering. Using this system, we compared the differences in platelet aggregability between 90 smoking healthy males after 10 hours of smoking abstinence and 141 age-matched nonsmoking healthy males. Smokers had more small spontaneous platelet aggregates and more medium and large aggregates induced by 1 or 5 microM of epinephrine than nonsmokers. No large aggregates with 5-microM epinephrine-induced platelet aggregation were seen in 10% of smokers and 24% of nonsmokers; these subjects showed no small aggregates in spontaneous aggregation at all. Smokers had significantly more small, medium, and large aggregates induced by 1 microM of adenosine diphosphate (ADP) than nonsmokers. Smokers showed a positive correlation between age and 1-microM epinephrine-induced large platelet aggregates, percent reduction of optical density, and 1-microM ADP-induced medium and large aggregates. Smokers also showed a positive correlation between fibrinogen concentration in plasma and small spontaneous aggregates. On the other hand, nonsmokers showed a significant positive correlation between age and small spontaneous aggregates, and a positive correlation between fibrinogen and 1- or 5-microM epinephrine-induced large aggregates, and between 1 microM ADP-induced large aggregates and percent reduction of optical density. These results confirmed that platelet aggregability is enhanced in smokers, and we speculate that long-term smoking might enhance the sensitivity of platelets to epinephrine or ADP.