McCulloch R K, Vandongen R
Department of Medicine, University of Western Australia, Royal Perth Hospital.
Prostaglandins. 1990 Jan;39(1):13-21. doi: 10.1016/0090-6980(90)90090-i.
The role of TXA2 in PAF-induced aggregation and secretion of human platelets is unclear. We have studied the relationship between aggregation, synthesis of TXA2 and release of 5-HT during the time course of aggregation induced by PAF and collagen. For PAF-induced aggregation there was strong aggregation and secretion with minimal production of TXA2 in contrast to collagen in which a surge in TXA2 synthesis preceded both aggregation and secretion. To determine the role of calcium flux in PAF-induced aggregation we have similarly studied the temporal relationships between aggregation, secretion and TXA2 synthesis for calcium ionophore A23187 induced aggregation but found these to be distinctly different from those determined for PAF. A method for measuring absolute amounts of 5HT released from platelets in small volumes of plasma is described. We conclude that TXA2 is not important in the mechanism of PAF induced aggregation and that an increase in the level of intraplatelet calcium per se is not sufficient to explain the mediation of PAF-induced aggregation.
血栓素A2（TXA2）在血小板活化因子（PAF）诱导的人血小板聚集和分泌过程中的作用尚不清楚。我们研究了在PAF和胶原蛋白诱导的聚集过程中，聚集、TXA2合成与5-羟色胺（5-HT）释放之间的关系。对于PAF诱导的聚集，有强烈的聚集和分泌，而TXA2的产生极少，这与胶原蛋白相反，在胶原蛋白诱导的聚集中，TXA2合成的激增先于聚集和分泌。为了确定钙内流在PAF诱导的聚集中的作用，我们同样研究了钙离子载体A23187诱导聚集时聚集、分泌和TXA2合成之间的时间关系，但发现这些与PAF诱导的聚集明显不同。本文描述了一种测量少量血浆中血小板释放的5-HT绝对量的方法。我们得出结论，TXA2在PAF诱导的聚集机制中并不重要，并且血小板内钙水平的升高本身不足以解释PAF诱导聚集的介导作用。
