Weiss C, Regele S, Velich T, Bärtsch P, Weiss T
Abteilung für Sportmedizin und Abteilung für Kardiologie/Angiologie, Universität Heidelberg, Heidelberg, Germany.
Prostaglandins Leukot Essent Fatty Acids. 2000 Nov;63(5):271-7. doi: 10.1054/plef.2000.0214.
There is evidence that the coagulation system is activated in patients with peripheral arterial occlusive disease (PAOD). The beneficial effects of the vasoactive drug prostaglandin E1 (PGE1) may rely in part on the modulation of the coagulation system. The study was designed to evaluate the effects of PGE1 on hemostatic and fibrinolytic variables in patients with intermittent claudication. Therefore molecular markers of thrombin (prothrombin fragment 1+2, PTF 1+2; thrombin-antithrombin III complexes, TAT) and fibrin formation (fibrinopeptide A, FPA) and markers of the fibrinolytic activity (fibrin degradation products, D-dimers) were determined before and immediately after the first PGE1 dose (60 microg in 100 ml NaCl over 2 h i.v.) as well as after 4 weeks of daily infusion therapy in 12 PAOD patients and in eight control patients before and after a single placebo infusion. Plasma levels of PTF1+2, TAT, FPA and D-dimers tended to decrease after the initial dose of PGE1. Infusion therapy with PGE1 for 4 weeks led to a decrease of all hemostatic and fibrinolytic parameters with most pronounced changes for PFT1+2, D-dimers and plasminogen activator inhibitor-1 decreasing by 11% (P<0.05), 20% (P<0.05), and 7% (P<0.05), respectively. These variables remained unchanged in controls with placebo infusion. In summary, infusion therapy with PGE1 in patients with PAOD reduces thrombin formation and results in a decrease of fibrin degradation. PGE1 may thus reduce fibrin deposition involved in the pathogenesis of atherosclerosis.
有证据表明，外周动脉闭塞性疾病（PAOD）患者的凝血系统被激活。血管活性药物前列腺素E1（PGE1）的有益作用可能部分依赖于对凝血系统的调节。本研究旨在评估PGE1对间歇性跛行患者止血和纤溶变量的影响。因此，在12例PAOD患者和8例对照患者中，在首次给予PGE1剂量（60μg溶于100ml NaCl中，静脉滴注2小时）之前、之后即刻以及每日输注治疗4周后，测定凝血酶（凝血酶原片段1 + 2，PTF 1 + 2；凝血酶 - 抗凝血酶III复合物，TAT）和纤维蛋白形成（纤维蛋白肽A，FPA）的分子标志物以及纤溶活性标志物（纤维蛋白降解产物，D - 二聚体），同时在8例对照患者单次输注安慰剂之前和之后进行测定。给予初始剂量的PGE1后，PTF1 + 2、TAT、FPA和D - 二聚体的血浆水平趋于下降。PGE1输注治疗4周导致所有止血和纤溶参数下降，其中PFT1 + 2、D - 二聚体和纤溶酶原激活物抑制剂 - 1变化最为明显，分别下降了11%（P < 0.05）、20%（P < 0.05）和7%（P < 0.05）。在输注安慰剂的对照患者中，这些变量保持不变。总之，PAOD患者输注PGE1治疗可减少凝血酶形成并导致纤维蛋白降解减少。因此，PGE1可能减少参与动脉粥样硬化发病机制的纤维蛋白沉积。
