Braun M, Schrör K
Institut für Pharmakologie, Heinrich-Heine-Universität Düsseldorf, FRG.
Stroke. 1990 Dec;21(12 Suppl):IV152-4.
Platelet activation results in the formation of various vasoactive mediators such as thromboxane A2 and serotonin. We investigated the effects of Bay U 3405 [(3R)-3- (4-fluorophenyl-sulfonamido)-1,2,3,4,-tetrahydro-9-carbazolepro panoic acid] on vasocontractions of isolated bovine cerebral arteries induced by U 46.619, a stable thromboxane/prostaglandin-endoperoxide analogue, and authentic thromboxane A2 released from thrombin-stimulated human platelets. Bay U 3405 (0.001-10 mumol/l) potently inhibited the contraction induced by U 46.619 and demonstrated a reduction of the thromboxane-mediated component of platelet-induced contractile response at higher concentrations (0.1-10 mumol).
血小板活化导致形成各种血管活性介质，如血栓素A2和5-羟色胺。我们研究了Bay U 3405 [（3R）-3-（4-氟苯基磺酰胺基）-1,2,3,4-四氢-9-咔唑丙酸]对由稳定的血栓素/前列腺素内过氧化物类似物U 46.619以及凝血酶刺激的人血小板释放的 authentic血栓素A2诱导的离体牛脑动脉血管收缩的影响。Bay U 3405（0.001 - 10 μmol/L）有效抑制U 46.619诱导的收缩，并在较高浓度（0.1 - 10 μmol）时显示出血小板诱导的收缩反应中血栓素介导成分的减少。
