Chesney C M, Pifer D D, Byers L W, Muirhead E E
Blood. 1982 Mar;59(3):582-5.
The effect of pure synthetic PAF (1-0-alkyl-2-acetyl-sn-glycero-3-phosphorylcholine) was studied in human platelets. PAF (0.2--2.0 micrograms/ml) produced a dose-dependent aggregation in human platelet-rich plasma (PRP) or platelet suspension obtained by gel-filtration (GFP). In addition, PAF (0.8 microgram/ml) induced secretion of 14C-serotonin (45% +/- 10%; mean +/- SD, n = 9) and platelet factor 4 (PF4) (12.89 +/- 3.81 micrograms/10(9) platelets; n = 9) in PRP. Similar results were obtained in GFP. Aggregation and release of 14C-serotonin and PF4 were inhibited by the metabolic inhibitors 2-deoxyglucose (16.7 mM) and antimycin-A (8.3 micrograms/ml), by the membrane-active drugs mepacrine (10 microM) and chlorpromazine (0.025 mM), by PGI2 (5.34 nM), which elevates intracellular c-AMP, by indomethacin (10 microM) or aspirin (100 microM). The ADP scavengers, creatine phosphate and creatine phosphokinase (CP/CPK), inhibited the second wave of aggregation but not secretion. These data suggest that the major effect of PAF on human platelets is mediated through the cyclo-oxygenase pathway and not through a third pathway.
研究了纯合成血小板活化因子（1-0-烷基-2-乙酰基-sn-甘油-3-磷酸胆碱）对人血小板的作用。血小板活化因子（0.2 - 2.0微克/毫升）在富含血小板的人血浆（PRP）或通过凝胶过滤获得的血小板悬液（GFP）中产生剂量依赖性聚集。此外，血小板活化因子（0.8微克/毫升）在PRP中诱导14C-5-羟色胺分泌（45%±10%；平均值±标准差，n = 9）和血小板因子4（PF4）（12.89±3.81微克/10^9个血小板；n = 9）。在GFP中也获得了类似结果。14C-5-羟色胺和PF4的聚集与释放受到代谢抑制剂2-脱氧葡萄糖（16.7毫摩尔）和抗霉素A（8.3微克/毫升）、膜活性药物米帕林（10微摩尔）和氯丙嗪（0.025毫摩尔）、升高细胞内c-AMP的前列环素（PGI2）（5.34纳摩尔）、吲哚美辛（10微摩尔）或阿司匹林（100微摩尔）的抑制。ADP清除剂磷酸肌酸和肌酸磷酸激酶（CP/CPK）抑制第二波聚集但不抑制分泌。这些数据表明，血小板活化因子对人血小板的主要作用是通过环氧化酶途径介导的，而不是通过第三条途径。
