The aim of this study was to investigate the in vivo effects of 50 mg/kg (i
.p.) naftazone or ticlopidine on platelet functions in the rat. An automate
d isotope monitoring system (Aims plus) nas used to determine the height of
platelet aggregation and disaggregation (measured hi. the area under the c
urve, AUC) of (111)indium-labelled platelets activated by ADP (10 mu g/kg i
.v.) or collagen (50 mu g/kg i.v.). Fibrinogen-binding experiments were car
ried out with activated platelets in whole blood and measured by flow cytom
etry. Naftazone reduced the height of platelet aggregation induced by ADP c
ompared with controls (P = 0.003). Ticlopidine-treated rats gave similar re
sults (P = 0.008). Platelet disaggregation, following the aggregation induc
ed by collagen, was significantly increased in naftazone-treated rats compa
red with controls (P = 0.003). Similar results were observed with ticlopidi
ne-treated rats (P = 0.002). Fibrinogen binding to 2.5 or 5 mu M ADP-stimul
ated platelets, from naftazone-treated rats, were significantly reduced com
pared with controls (P = 0.05 and 0.01 respectively). These results show th
at naftazone has similar inhibitory effects on rat platelet functions as ti
cloplidine. In conclusion, naftazone could be a useful agent to modulate pl
atelet function in patients with cardiovascular disease.