Nishizawa E E, Williams D J, Connell C L
Thromb Res. 1983 May 1;30(3):289-96. doi: 10.1016/0049-3848(83)90082-8.
Platelet aggregation was measured in rat and human platelet-rich plasma (PRP) after the addition of various amounts of arachidonic acid (AA), prostaglandin H2 (PGH2), adenosine diphosphate (ADP), or collagen. AA but not PGH2 caused rat platelets to aggregate in citrated or heparinized PRP. Both AA and PGH2 produced significant amounts of thromboxane A2 (TxA2) measured as thromboxane B2 (TxB2). The lack of aggregation of rat platelets with PGH2 was not due to the formation of an inhibitor of aggregation such as a prostaglandin. Thus, the formation of TxA2 may not be necessary for aggregation of rat platelets. Human platelets were aggregated by PGH2 with the concomitant formation of TxB2.
在添加不同量的花生四烯酸（AA）、前列腺素H2（PGH2）、二磷酸腺苷（ADP）或胶原蛋白后，测定大鼠和人富含血小板血浆（PRP）中的血小板聚集情况。AA可使枸橼酸化或肝素化PRP中的大鼠血小板聚集，而PGH2则不能。AA和PGH2均可产生大量以血栓素B2（TxB2）衡量的血栓素A2（TxA2）。大鼠血小板与PGH2不发生聚集并非由于形成了如前列腺素等聚集抑制剂。因此，TxA2的形成可能并非大鼠血小板聚集所必需。PGH2可使人类血小板聚集，并伴随TxB2的形成。
