Szczeklik A, Gryglewski R J, Musiał J, Grodzińska L, Serwońska M, Marcinkiewicz E
Thromb Haemost. 1978 Aug 31;40(1):66-74.
Arachidonic acid (AA)-induced platelet aggregation was studied in platelet-rich plasma of 30 male patients who survived myocardial infarction and in 30 healthy men of similar age. Mean platelet aggregation thresholds to AA were 746 +/- 62 micrometer, and 869 +/- 57 micrometer, respectively. Only in 2 healthy subjects, but in 12 patients, irreversible platelet aggregation was induced consistently with low concentrations of AA, under 500 micrometer. The rate of conversion of AA to thromboxane A2 (TXA2) by platelets of these patients was augmented. Furthermore, less endogenous TXA2 was required to trigger aggregation of their platelets as compared to the controls. We have also shown that in platelet-poor plasma of these patients with "hyperreactive" platelets there exists a transferable factor which makes platelets of healthy subjects more prone to aggregatory action of AA. It is proposed that the assessment of platelet aggregability with AA provides a tool for identifying a subgroup of patients with coronary heart disease who might substantially benefit from the secondary preventive treatment with aspirin and with other antiplatelet drugs which inhibit the generation of TXA2 in platelets.
在30名心肌梗死存活男性患者及30名年龄相仿的健康男性的富血小板血浆中研究了花生四烯酸（AA）诱导的血小板聚集情况。AA诱导的平均血小板聚集阈值分别为746±62微米和869±57微米。仅在2名健康受试者中，但在12名患者中，低浓度（低于500微米）的AA可持续诱导不可逆的血小板聚集。这些患者血小板将AA转化为血栓素A2（TXA2）的速率增加。此外，与对照组相比，触发其血小板聚集所需的内源性TXA2更少。我们还表明，在这些具有“高反应性”血小板的患者的贫血小板血浆中存在一种可转移因子，该因子使健康受试者的血小板更易于AA的聚集作用。有人提出，用AA评估血小板聚集性可为识别冠心病患者亚组提供一种工具，这些患者可能从阿司匹林及其他抑制血小板中TXA2生成的抗血小板药物的二级预防治疗中显著获益。
