P217 Smoking is assumed to be a risk factor in stroke-patients. Ticlopidine or ASA should prevent from stroke by inhibition of platelet function. Platelet function i.e. platelet reactivity (PR) (Grotemeyer, Thrombosis research 63;587) was determined before and after smoking without drugs, 2 hours after intake of ASA or ticlopidine and 5 days after loading with 2 x 250 mg ticlopidine/day . At each experiment 3 cigarettes (Marlboro ®) were smoked within 30 min. Blood was collected immediately before smoking and 30 min later. A washout period of 14 days was between each drug-experiment. Included were 23 healthy male smokers (age 25,2 ± 3,3 yr.) PR (before smoking) was 1.15 ± 0,15, after smoking 1,42 ± 0,18. Average difference (AD)(PR after - PR before smoking) was 0,28 ± 0,13. Pathological PR-values (>1.25) were seen in 95% of the smokers after the experiment. (Wilcoxon p<0,001) Two hours after intake of 500 mg ASA the AD was 0,13 ± 0,20. 60% of the values became pathological after smoking (p<0,01). Two hours after once 250 mg ticlopidine AD was 0,007 ± 0,16, 10% of the PR-values became pathological (n.s.). After 4 hours: AD =0,025 ± 0,04, after 6 hours: AD = 0,07 ± 0,04, after 8 hours: AD = 0,123 +/- 0,08 and 90% of the smokers showed pathological values (p<0,01). After the 5 day loading and 2 h after 250 mg ticlopidine AD was -0,01 ± 0,26, 5% PR-values became pathological (n.s.), after 4 h: AD = 0,05 ± 0,12, after 6 h: AD = 0,07 ± 0,07, after 8 h AD = 0,04 ± 0,05. 76% showed pathological values. AD after 10 h = 0,23 ± 0,27 Based on the percentage of smokers with pathological values the logrank-test showed with p<0,001 a significant difference in the ticlopidine experiments in favor to the testing after a loading time. Even if ticlopidine seems to be more effective as compared to ASA, it cannot be assumed that the drug - from the laboratory point of view - can compensate the negative activating effect of smoking on platelets completely.