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苄环烷对血小板体外和体内聚集的抑制活性(作者译)

[Inhibitory activity of bencyclan on platelet aggregation in vitro and in vivo (author's transl)].

作者信息

Jäger W, Scharrer I, Satkowski U, Breddin K

出版信息

Arzneimittelforschung. 1975;25(12):1938-44.

PMID:1243666
Abstract

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.

摘要

N-[3-(苄基-环庚氧基)-丙基]-N,N-二甲基胺(苄环烷氢富马酸盐,氟地西泮)在检测自发聚集活性(PAT I - III)的试验中,以10⁻⁵摩尔浓度抑制自发增强的聚集。苄环烷还抑制血小板黏附以及ADP或胶原诱导的血小板聚集。10⁻⁵ M的苄环烷可引起血小板轻微肿胀,5×10⁻⁴ Mol则完全抑制触须形成,若用干涉相差显微镜观察,可使血小板转变为小球形。苄环烷诱导的形态学改变可能是其对体外不同血小板功能试验产生抑制作用的原因。每天口服300 - 600 mg苄环烷在体内并不抑制血小板聚集。在聚集倾向增强的患者中,静脉注射200 - 400 mg苄环烷可导致血小板聚集的短期抑制,通常持续时间不超过1小时。未发现¹⁴C标记的苄环烷与血小板结合。在体外和体内,一些¹⁴C标记的苄环烷与白蛋白结合。

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