Meringolo C, Bartolini G, Orlandi M, Tomasi V, Barnabei O
Prostaglandins Med. 1979 May;2(5):381-92. doi: 10.1016/0161-4630(79)90111-3.
Endoperoxide analogs at doses 100-fold higher than those required to aggregate human platelet-rich plasma (PRP), were ineffective on rat PRP. Indomethacin (20 microM) and imidazole did not affect arachidonate-induced aggregation of rat PRP. On the other hand, prostaglandin (PG) E1 inhibited aggregation at doses similar to those effective on human PRP, while high doses of PGI2 failed to inhibit arachidonate aggregation in the rat. Eicosatetraynoic acid (10 microgram) blocked the second phase of aggregation; the Ca2+-ionophore A 23187 potentiated the arachidonate effect. Thus, it appears that endoperoxides or thromboxane A2 may not be involved in rat platelet aggregation and that the formation of aggregants from arachidonate shares many properties with the biosynthesis of slow reacting substance, a metabolite of arachidonic acid containing a sulphate group. To test this, rat PRP was incubated with labeled sulphate and aggregated with arachidonate. After column and thin layer chromatography a labeled lipid was identified having a mobility higher than phospholipids but lower than PGF2 alpha. Treatment with arylsulphatase decreased radioactivity by at least 70%.
内过氧化物类似物的剂量比聚集人富血小板血浆（PRP）所需剂量高100倍时，对大鼠PRP无效。吲哚美辛（20微摩尔）和咪唑不影响花生四烯酸诱导的大鼠PRP聚集。另一方面，前列腺素（PG）E1以与对人PRP有效的剂量相似的剂量抑制聚集，而高剂量的前列环素（PGI2）未能抑制大鼠中的花生四烯酸聚集。二十碳四炔酸（10微克）阻断聚集的第二阶段；钙离子载体A 23187增强了花生四烯酸的作用。因此，似乎内过氧化物或血栓素A2可能不参与大鼠血小板聚集，并且由花生四烯酸形成聚集剂与含有硫酸基团的花生四烯酸代谢产物慢反应物质的生物合成具有许多共同特性。为了验证这一点，将大鼠PRP与标记的硫酸盐一起孵育，并用花生四烯酸聚集。经过柱色谱和薄层色谱后，鉴定出一种标记的脂质，其迁移率高于磷脂但低于PGF2α。用芳基硫酸酯酶处理使放射性至少降低70%。
