Kinlough-Rathbone R L, Packham M A
Department of Pathology, McMaster University, Hamilton, Ontario, Canada.
Thromb Haemost. 1992 Aug 3;68(2):189-93.
Aurin tricarboxylic acid (ATA) is a potent inhibitor of ristocetin-mediated platelet agglutination and of shear-induced, von Willebrand factor (vWf)-mediated platelet aggregation, probably via inhibition of vWf interaction with glycoprotein Ib (GPIb). We examined the effects of ATA (both the sodium salt and a solution of ATA in ethanol) on platelet functions in citrated plasma (PRP) and in suspensions of washed platelets in Tyrode-albumin solution (contains 2 mM Ca2+). ATA (42-211 micrograms/ml) blocked aggregation and release of granule contents induced by thrombin (0.15 U/ml in PRP; 0.03 U/ml in platelet suspension). Responses to higher concentrations of thrombin were not inhibited. ATA also prolonged thrombin-induced clotting of fibrinogen. Since ATA had no effect on fibrinogen-induced responses of chymotrypsin-treated platelets, ATA probably acts on thrombin rather than on fibrinogen. In PRP and platelet suspensions, ATA (acid form 106 micrograms/ml; sodium salt 122 micrograms/ml) had little effect on ADP-induced platelet aggregation. The sodium salt of ATA (61-122 micrograms/ml) enhanced collagen-induced aggregation and release by platelets in citrated plasma and by washed platelets; the enhancement was extensively inhibited by aspirin. With platelet suspensions, ATA significantly enhanced aggregation and release caused by low concentrations of sodium arachidonate (15-50 microM); aggregation and release caused by higher concentrations of arachidonate were somewhat inhibited by ATA. Arachidonate-induced aggregation and release were also enhanced by ATA in PRP. ATA enhanced aggregation and release induced by the calcium ionophore A23187; aspirin had little effect on the enhancement.(ABSTRACT TRUNCATED AT 250 WORDS)
金精三羧酸（ATA）是瑞斯托菌素介导的血小板凝集以及剪切诱导的、血管性血友病因子（vWf）介导的血小板聚集的强效抑制剂，可能是通过抑制vWf与糖蛋白Ib（GPIb）的相互作用。我们研究了ATA（钠盐以及ATA的乙醇溶液）对枸橼酸盐血浆（富血小板血浆，PRP）以及在Tyrode-白蛋白溶液（含2 mM Ca2+）中的洗涤血小板悬液中血小板功能的影响。ATA（42 - 211微克/毫升）可阻断凝血酶（PRP中为0.15 U/毫升；血小板悬液中为0.03 U/毫升）诱导的颗粒内容物的聚集和释放。对更高浓度凝血酶的反应未被抑制。ATA还延长了凝血酶诱导的纤维蛋白原凝血时间。由于ATA对胰凝乳蛋白酶处理的血小板的纤维蛋白原诱导反应无影响，所以ATA可能作用于凝血酶而非纤维蛋白原。在PRP和血小板悬液中，ATA（酸形式为106微克/毫升；钠盐为122微克/毫升）对ADP诱导的血小板聚集影响很小。ATA的钠盐（61 - 122微克/毫升）增强了枸橼酸盐血浆中的血小板以及洗涤血小板对胶原诱导的聚集和释放；阿司匹林可广泛抑制这种增强作用。对于血小板悬液，ATA显著增强了低浓度花生四烯酸钠（15 - 50 microM）引起的聚集和释放；较高浓度花生四烯酸引起的聚集和释放受到ATA的一定抑制。花生四烯酸诱导的聚集和释放在PRP中也被ATA增强。ATA增强了钙离子载体A23187诱导的聚集和释放；阿司匹林对这种增强作用影响很小。（摘要截短于250字）
