Van Nueten J M, De Ridder W, Van Gorp L, De Clerck F
Eur J Pharmacol. 1987 Jan 20;133(3):301-8. doi: 10.1016/0014-2999(87)90026-4.
Human blood platelets, stimulated with thrombin, induced contractions of isolated basilar artery segments of the dog. These platelet-mediated vascular contractions were inhibited in a concentration-dependent way by flunarizine, a Ca2+ entry blocker, selective for vascular tissues (IC50: 5.5 X 10(-7) M). This inhibition increased gradually as a function of the time contact with flunarizine, to reach its maximum after 60-90 min. Biochemical and pharmacological analyses using the S2-serotonin receptor antagonist ritanserin, the thromboxane A2/prostaglandin endoperoxide antagonist BM 13.177 and the fatty acid cyclo-oxygenase inhibitor suprofen showed that 5-hydroxytryptamine and prostanoids (thromboxane A2, prostaglandin endoperoxides) were the main mediators involved. The results further suggested amplification between the vascular effects of 5-hydroxytryptamine and prostanoids. Flunarizine did not affect the release of 5-hydroxytryptamine from platelets and did not interfere with their biosynthesis of thromboxane A2.
用凝血酶刺激人血小板，可引起犬离体基底动脉节段收缩。这些由血小板介导的血管收缩，被氟桂利嗪以浓度依赖的方式抑制，氟桂利嗪是一种对血管组织有选择性的Ca2+内流阻滞剂（IC50：5.5×10(-7)M）。这种抑制作用随着与氟桂利嗪接触时间的延长而逐渐增强，在60 - 90分钟后达到最大值。使用5-羟色胺受体拮抗剂利坦色林、血栓素A2/前列腺素内过氧化物拮抗剂BM 13.177以及脂肪酸环氧化酶抑制剂舒洛芬进行的生化和药理学分析表明，5-羟色胺和前列腺素类（血栓素A2、前列腺素内过氧化物）是主要的介导因子。结果还提示5-羟色胺和前列腺素类的血管效应之间存在放大作用。氟桂利嗪不影响血小板释放5-羟色胺，也不干扰其血栓素A2的生物合成。
