[Possibility of regulating platelet aggregation ability with the S2-receptor blocker, naftidrofuril, in patients with insulin-dependent diabetes mellitus].

The actions of S2-receptor antagonist naftidrofuril (Duzodril-retard, Byk Gulden, FRG) on both basal and thrombin-induced levels of malondialdehyde in platelets as well as platelet aggregability in patients with insulin-dependent diabetes mellitus with or without angiopathies were studied. Significant decrease in the basal level of MDA was observed after treatment and the effect was more profound in patients without vascular complications. The treatment with Duzodril-retard at daily dose of 200 mg during 40 days was not shown to decrease in platelet hyperfunction in response to the inductors: ADP, 1 and 5 microM; adrenaline, 1 microM; collagen, 4 mu/ml; ristomycin, 0.9 and 1.2 mg/ml; and thrombin 0.5 U/ml). The reduction of hyperreactivity of platelets in response to adrenaline in patients without angiopathies was found out during treatment with Duzodril-retard. This could be referred as positive sign for prognosis because of decrease in sensitivity of platelets to adrenaline may lead to corresponding decrease in reactivity to ADP during long-term usage of naftidrofuril. Platelets of the patients were shown to be hypersensitive to ADP at maximal extent. The decrease in the sensitivity of platelets to large concentrations of ristomycin was found, the fact which may serve as an evident for some normalization of functional activity of platelets as well endothelin-platelet interactions in patients without vasal complications. Thus, Duzodril-retard has an activity as angio-protector in most degree at the cases when vasal disturbances are not clinically significant yet.