Iatridis P G, Hadd H, Kotrotsou M, Iatridis S G
Thromb Res. 1986 Apr 15;42(2):177-85. doi: 10.1016/0049-3848(86)90293-8.
We have investigated the effects of 2,3-DPG on platelet aggregation in the presence of suboptimal concentrations of Na-Arachidonate by using the two cuvette transfer experiments of Hamberg, Svensson and Samuelsson (3). The results show that 2,3-DPG enhanced or induced platelet aggregation in the presence of suboptimal concentrations of Na-Arachidonate. Imidazole, a TXA2 synthetase inhibitor, and Lasix, when added inhibited 2,3-DPG effects on platelet aggregation, suggesting that 2,3-DPG may act either on cyclooxygenase or on TXA2 synthetase of prostaglandin synthesis. A specific RIA assay showed that 2,3-DPG when added to suboptimal concentrations of Na-Arachidonate enhanced the formation of TXB2, a stable metabolite of TXA2. We have concluded that during intravascular hemolysis 2,3-DPG release may be a key component in preventing and/or inducing thrombosis.
我们采用哈姆贝格、斯文森和萨缪尔森的双比色皿转移实验（3），研究了在次优浓度花生四烯酸钠存在下2,3-二磷酸甘油酸（2,3-DPG）对血小板聚集的影响。结果表明，在次优浓度花生四烯酸钠存在下，2,3-DPG增强或诱导了血小板聚集。添加血栓素A2（TXA2）合成酶抑制剂咪唑和速尿后，抑制了2,3-DPG对血小板聚集的作用，这表明2,3-DPG可能作用于前列腺素合成的环氧化酶或TXA2合成酶。一种特定的放射免疫分析表明，当向次优浓度的花生四烯酸钠中添加2,3-DPG时，会增强TXA2的稳定代谢产物血栓素B2（TXB2）的形成。我们得出结论，在血管内溶血过程中，2,3-DPG的释放可能是预防和/或诱导血栓形成的关键因素。
