Saniabadi A R, Lowe G D, Barbenel J C, Forbes C D
Thromb Haemost. 1984 Feb 28;51(1):115-8.
ADP, generated from red blood cells is believed to be responsible for the spontaneous aggregation of platelets in whole blood. This notion is based mainly on the use of enzymes which remove ADP. We have studied spontaneous platelet aggregation in whole blood and autologous platelet rich plasma obtained from 12 healthy male and female volunteers. Platelet aggregation was quantitated by measuring the fall in the number of single platelets counted using a whole blood platelet counter (Ultra Flo 100). In a rotating tube model, the mean fall in the number of platelets due to spontaneous aggregation was 56% in whole blood but, only 3% in platelet rich plasma prepared from the same blood samples. Spontaneous platelet aggregation in whole blood was unaffected by apyrase grade I, but was reduced to 15% by apyrase grade II, to 38% by creatine phosphokinase/creatine phosphate and to 9% by pyruvate kinase/phosphoenolpyruvate. The results of this study provide additional evidence that ADP generated in whole blood triggers the spontaneous aggregation of platelets.
红细胞生成的二磷酸腺苷（ADP）被认为是全血中血小板自发聚集的原因。这一观点主要基于使用去除ADP的酶的研究。我们研究了从12名健康男性和女性志愿者采集的全血和自体富血小板血浆中的血小板自发聚集情况。使用全血血小板计数器（Ultra Flo 100）通过测量单个血小板数量的下降来定量血小板聚集。在旋转管模型中，全血中由于自发聚集导致的血小板数量平均下降为56%，但从相同血样制备的富血小板血浆中仅为3%。全血中的血小板自发聚集不受I级腺苷三磷酸双磷酸酶的影响，但被II级腺苷三磷酸双磷酸酶降低至15%，被肌酸磷酸激酶/磷酸肌酸降低至38%，被丙酮酸激酶/磷酸烯醇丙酮酸降低至9%。本研究结果提供了额外证据，表明全血中生成的ADP触发血小板的自发聚集。
