1. In view of the importance of 5-hydroxytryptamine in coronary thrombosis, we wanted to know whether a potentially protective decrease in platelet 5-hydroxytryptamine could be achieved by treatment with an inhibitor of 5-hydroxytryptamine uptake, fluoxetine. 2. We studied 15 patients treated for psychiatric indications with fluoxetine, and compared the findings with those obtained with blood from 18 patients treated with amitriptyline and 13 controls previously treated for affective disorders. 3. Platelet-rich plasma 5-hydroxytryptamine levels were significantly decreased in the fluoxetine group (P < 0.005) but not in the amitriptyline group compared with the control group. 4. Collagen-induced aggregation in whole blood anticoagulated with hirudin was measured by sequential single platelet counting. The contribution of 5-hydroxytryptamine was assessed from the effect of adding the 5-hydroxytryptamine specific antagonist ICI 170809. This contribution was significantly decreased in the fluoxetine group but not in the amitriptyline group compared with the control group. 5. It is concluded that platelet 5-hydroxytryptamine is indeed decreased by fluoxetine, and we would predict a protective effect of fluoxetine against coronary thrombosis.

7Panti-PDGF-BB and anti-bFGF were maintained a t levels approximately 10-fold higher than those required t o neutralise the mitogenic and chemotactic effects of 5 ng/ ml o f PDGF-BB, or bFGF in-vitro. Used singly, anti-PDGF IgG treatment (n=8) was associated with a 55.6% reduction i n intimal area and a 48.7% reduction i n intimal: medial area ratio; anti-bFGF IgG administration (n.8) caused a 55.6% reduction intimal area, and a 50.1% reduction i n intimal: medial area ratio. Treatment with a combination of these antibodies (n.9) resulted in a 89% reduction in intimal area (p