Ulutin O N, Balkuv-Ulutin S, Bezer-Göker B, Cizmeci G, Ferhanoğlu B, Ozsoy Y, Uğur M S, Ulutin T, Yaman A, Yardimci T
Thrombosis and Hemostasis Research Center, Cerrahpaşa Medical School of Istanbul University, Turkey.
Semin Thromb Hemost. 1996;22 Suppl 1:21-4.
Defibrotide, a polydeoxyribonucleotide, has been found to modulate endothelial cell function, causing an increase in tissue plasminogen activator (t-PA) levels, a decrease in plasminogen activator inhibitor (PAI) levels, and an increase in prostaglandin I2 (PGI2) formation in humans. Defibrotide has no direct anticoagulant effect but has a synergistic action with heparin. A strong antithrombotic effect has been observed in animal models. Thus, defibrotide has a beneficial effect in cases of deep venous thrombosis (DVT), peripheral obliterative vascular disorder (POVD), stroke, vasculitis, and thromboembolism. Defibrotide also inhibits platelet function and activation. A significant decrease in platelet aggregate formation on the suture line in microarterial anastomosis in rats is one way defibrotide can inhibit platelet function and activation. In humans, a slight prolongation' of the lag period in collagen-induced aggregation has been observed. In addition, a slight decrease in the maximum amplitude of the secondary wave of ADP and adrenalin-induced aggregations was also found. Platelet adhesion is diminished, the platelet differential count on formvar membrane is altered, and platelet aggregate formation is significantly inhibited. With an increase in platelet cyclic AMP (cAMP) content and a decrease in malonyl dialdehyde (MDA) and thromboxane B2 (TXB2) formation, the levels of platelet secretion products such as PF-4 and beta-thromboglobulin (beta-TG) in plasma decreased progressively. It was also demonstrated that the 14C-glucose transport defect of the platelet membrane of atherosclerotic patients was partially corrected with defibrotide treatment.
去纤苷是一种多脱氧核糖核苷酸，已发现它可调节内皮细胞功能，使人体组织型纤溶酶原激活剂（t-PA）水平升高、纤溶酶原激活剂抑制剂（PAI）水平降低，并使前列腺素I2（PGI2）生成增加。去纤苷没有直接的抗凝作用，但与肝素具有协同作用。在动物模型中已观察到其强大的抗血栓形成作用。因此，去纤苷对深静脉血栓形成（DVT）、周围闭塞性血管疾病（POVD）、中风、血管炎和血栓栓塞病例具有有益作用。去纤苷还可抑制血小板功能和活化。大鼠微动脉吻合术缝线处血小板聚集形成显著减少是去纤苷抑制血小板功能和活化的一种方式。在人体中，已观察到胶原诱导聚集的延迟期略有延长。此外，还发现ADP和肾上腺素诱导聚集的次级波最大振幅略有降低。血小板黏附减少，福尔马膜上的血小板分类计数改变，血小板聚集形成受到显著抑制。随着血小板环磷酸腺苷（cAMP）含量增加以及丙二醛（MDA）和血栓素B2（TXB2）生成减少，血浆中血小板分泌产物如PF-4和β-血小板球蛋白（β-TG）水平逐渐降低。还证明，去纤苷治疗可部分纠正动脉粥样硬化患者血小板膜的14C-葡萄糖转运缺陷。
