Abbate R, Gori A M, Martini F, Attanasio M, Comeglio P, Giusti B, Zarone N, Francalanci I, Prisco D, Gensini G F
Clinica Medica l e Cardiologia, University of Florence, Italy.
Semin Thromb Hemost. 1995;21(2):245-50. doi: 10.1055/s-2007-1000400.
Defibrotide is a polydeoxyribonucleotide-derived anti-ischemic drug with multiple sites of action involving both plasmatic and cellular targets. This agent has been demonstrated to produce profibrinolytic, cytoprotective, and vaso-facilatory actions. Since monocytes are increased in the mediation of some of the pathophysiologic responses seen in ischemic disorders, the functional properties of these cells were investigated in experimental conditions to evaluate their behavior during resting and stimulated states. Defibrotide was supplemented in these systems to determine its modulatory action. In this investigation Defibrotide was found to decrease the PAI-1 levels and may indicate that this may be the mechanism for its profibrinolytic actions. Defibrotide was also found to reduce the procoagulant activity of monocytes in these experimental settings. Both PAI and procoagulant factors play an important role in the pathophysiology of inflammation, DIC, and ischemia. Defibrotide induced reduction of these two factors represents the mechanism whereby this agent produces its therapeutic action.
去纤苷是一种源自多聚脱氧核糖核苷酸的抗缺血药物，具有多个作用位点，涉及血浆和细胞靶点。已证明该药物具有促纤溶、细胞保护和血管舒张作用。由于单核细胞在缺血性疾病的一些病理生理反应介导中增加，因此在实验条件下研究了这些细胞的功能特性，以评估它们在静息和刺激状态下的行为。在这些系统中添加去纤苷以确定其调节作用。在这项研究中，发现去纤苷可降低纤溶酶原激活物抑制剂-1（PAI-1）水平，这可能表明这是其促纤溶作用的机制。在这些实验环境中还发现去纤苷可降低单核细胞的促凝血活性。PAI和促凝血因子在炎症、弥散性血管内凝血（DIC）和缺血的病理生理学中均起重要作用。去纤苷诱导这两种因子的减少代表了该药物产生治疗作用的机制。
