Enhanced platelet aggregation as a risk factor for vascular disease and its thromboembolic complications.
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Biomedical subjects
Publications and source records attributed to K Breddin.
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N-[3-(Benzyl-cycloheptyloxy)-propyl]-N,N-dimethyl-amine (bencyclan-hydrogenfumarate, Fludilat¿) inhibits spontaneously enhanced aggregation in the tests which detect a spontaneous aggregating activity (PAT I--III) in 10(-5) molar concentration. Bencyclan also inhibits platelet adhesiveness and ADP or collagen induced platelet aggregation. 10(-5) M of bencyclan induced a slight swelling of platelets 5 times 10(-4) Mol inhibited the formation of tentacles completely and transformed the platelets into small spheres if investigated with interference-phase contrast microscopy. It is likely that the morphologic changes induced by bencyclan are responsible for the inhibitory effect on the different platelet function tests in vitro. In vivo oral application of 300-600 mg of bencyclan per day did not inhibit platelet aggregation. In patients with enhanced aggregating tendency i.v. injection of 200-400 mg bencyclan led to a short-time inhibition of platelet aggregation which usually did not last for more than 1 h. No binding of 14C-labelled bencyclan to platelets was found. In vitro and in vivo some 14C-labelled bencyclan was bound to albumins.
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