Sturk A, Asyee G M, Schaap M C, van Maanen M, ten Cate J W
Thromb Res. 1985 Nov 1;40(3):359-72. doi: 10.1016/0049-3848(85)90271-3.
The synergistic effects of platelet-activating factor (PAF) with ADP, collagen, thrombin, A23187, adrenaline, sodium arachidonate and ristocetin in human platelet aggregation and beta-thromboglobulin (beta-TG) release were investigated in citrated platelet-rich plasma (PRP). Synergism in both aggregation and release was present with all agonists except ristocetin. Upon oral intake of aspirin (ASA) the PAF-induced irreversible aggregation as well as the synergistic irreversible aggregation became reversible. Both prior to and after ASA ingestion ADP removal by creatine phosphate/creatine phosphokinase (CP/CPK) resulted in a reduced, reversible platelet aggregation induced by PAF alone or in combination with the other agonists. The ADP-removal and ASA-ingestion also strongly inhibited the beta-TG release. The synergistic aggregation and release were also inhibited by ASA and indomethacin in vitro as well as by the competitive ADP-inhibitor ATP. It is concluded that not only the activation of human platelets by low doses of PAF itself, but also the synergism of PAF and other platelet agonists is highly dependent upon ADP and products of the cyclooxygenase pathway.
在枸橼酸化富血小板血浆（PRP）中研究了血小板活化因子（PAF）与ADP、胶原、凝血酶、A23187、肾上腺素、花生四烯酸钠和瑞斯托菌素在人血小板聚集及β-血小板球蛋白（β-TG）释放方面的协同作用。除瑞斯托菌素外，所有激动剂在聚集和释放方面均存在协同作用。口服阿司匹林（ASA）后，PAF诱导的不可逆聚集以及协同不可逆聚集均变为可逆。在摄入ASA之前和之后，通过磷酸肌酸/磷酸肌酸激酶（CP/CPK）去除ADP均导致单独PAF或与其他激动剂联合诱导的血小板聚集减少且可逆。去除ADP和摄入ASA也强烈抑制β-TG的释放。协同聚集和释放也在体外被ASA和吲哚美辛以及竞争性ADP抑制剂ATP所抑制。结论是，不仅低剂量PAF本身对人血小板的激活，而且PAF与其他血小板激动剂的协同作用高度依赖于ADP和环氧化酶途径的产物。
