Because of the considerable interest in the role of platelets and antiplatelet
therapy in
cardiovascular disease, including the aggregation of platelets to each other during arterial
thrombosis and
atherogenesis, we have studied the effect of
naftazone (
Etioven), an original vasculotropic
drug on platelet aggregation. Rat and human platelets were prepared and incubated in-vitro with different concentrations of
naftazone. We found that
naftazone inhibited both platelet secretion and aggregation in platelet-rich plasma (PRP) and washed platelets after stimulation with
thrombin or
ADP. Rats were also treated intraperitoneally for five days with various
naftazone doses (0.125-10 mg kg-1) and ex-vivo platelet aggregation compared, at various times after the last injection, with that of control animals. Inhibition by
naftazone was dose-dependent in both PRP and isolated platelets. The inhibition was transient, a maximum value (approximately 50%) being obtained about 3-6 h after the last injection, with a return to near-control values after 24 h.
Naftazone also facilitated platelet deaggregation after in-vitro stimulation with
thrombin or
ADP. In another series of experiments, rats were treated intraperitoneally for five days with 10 mg kg-1 of
aspirin,
ticlopidine,
dipyridamole or
naftazone. Platelets were prepared and tested for aggregation 90 min after the last injection.
Thrombin-induced aggregation in PRP and washed platelets was significantly reduced after in-vivo treatment with
ticlopidine and
naftazone. Except for
dipyridamole, all the drugs inhibited ex-vivo
ADP-induced aggregation in PRP. In isolated platelet preparation, only
naftazone induced a significant inhibition of
ADP- or
thrombin-stimulated aggregation. We conclude that
naftazone inhibits platelet aggregation in-vitro and ex-vivo.