IN-VITRO AND EX-VIVO INHIBITION OF BLOOD-PLATELET AGGREGATION BY NAFTAZONE

Because of the considerable interest in the role of platelets and anti platelet therapy in cardiovascular disease, including the aggregation of platelets to each other during arterial thrombosis and atherogenesi s, we have studied the effect of naftazone (Etioven), an original vasc ulotropic drug on platelet aggregation. Rat and human platelets were p repared and incubated in-vitro with different concentrations of naftaz one. We found that naftazone inhibited both platelet secretion and agg regation in platelet-rich plasma (PRP) and washed platelets after stim ulation with thrombin or ADP. Rats were also treated intraperitoneally for five days with various naftazone doses (0.125-10 mg kg(-1)) and e x-vivo platelet aggregation compared, at various times after the last injection, with that of control animals. Inhibition by naftazone was d ose-dependent in both PRP and isolated platelets. The inhibition was t ransient, a maximum value (similar to 50%) being obtained about 3-6 h after the last injection, with a return to near-control values after 2 4 h. Naftazone also facilitated platelet deaggregation after in-vitro stimulation with thrombin or ADP. In another series of experiments, ra ts were treated intraperitoneally for five days with 10 mg kg(-1) of a spirin, ticlopidine, dipyridamole or naftazone. Platelets were prepare d and tested for aggregation 90 min after the last injection, Thrombin -induced aggregation in PRP and washed platelets was significantly red uced after in-vivo treatment with ticlopidine and naftazone. Except fo r dipyridamole, all the drugs inhibited ex-vivo ADP-induced aggregatio n in PRP. In isolated platelet preparation, only naftazone induced a s ignificant inhibition of ADP- or thrombin-stimulated aggregation. We c onclude that naftazone inhibits platelet aggregation in-vitro and ex-v ivo.