Hardisty R M, Powling M J, Nokes T J
Institute of Child Health, London, United Kingdom.
Thromb Haemost. 1990 Aug 13;64(1):150-5.
The effects on platelet function of a 5-day course of Ticlopidine (Tcl) have been studied in two groups of volunteers receiving different dosage schedules. Tcl had a relatively greater inhibitory effect on aggregation induced by ADP than by other agonists, and a greater effect, in contrast to that of an ADP receptor antagonist, on the second phase than on the initial rate of aggregation. Tcl inhibited ATP secretion in response to ADP and 0.05 u/ml thrombin, but not to higher concentrations of thrombin or to calcium ionophores. No inhibitory effect was observed on Ca2+ influx or intracellular mobilization, on the binding of monoclonal antibodies to the glycoprotein IIb-IIIa complex or on the state of association of the complex. We suggest that Tcl neither inhibits the binding of ADP to its receptor nor acts directly on the fibrinogen binding site, but that it may inhibit a step in signal transduction between these two events.
在两组接受不同给药方案的志愿者中，研究了为期5天的噻氯匹定（Tcl）疗程对血小板功能的影响。与其他激动剂相比，Tcl对ADP诱导的聚集具有相对更强的抑制作用，并且与ADP受体拮抗剂相比，对聚集的第二阶段的作用比对初始聚集速率的作用更大。Tcl抑制对ADP和0.05 U/ml凝血酶的ATP分泌，但对更高浓度的凝血酶或钙离子载体则无抑制作用。未观察到对Ca2+内流或细胞内动员、单克隆抗体与糖蛋白IIb-IIIa复合物的结合或该复合物的缔合状态有抑制作用。我们认为，Tcl既不抑制ADP与其受体的结合，也不直接作用于纤维蛋白原结合位点，但它可能抑制这两个事件之间信号转导的一个步骤。
