Takahashi H, Tatewaki W, Wada K, Niwano H, Hanano M, Shibata A
Department of Internal Medicine, Niigata University School of Medicine, Japan.
Am J Hematol. 1991 Apr;36(4):255-8. doi: 10.1002/ajh.2830360406.
Desmopressin acetate (DDAVP) is known to stimulate the release of tissue-type plasminogen activator (t-PA) from endothelial cells, but it is unclear whether the increased t-PA actually elicits the plasmin generation and fibrin(ogen)olysis in the circulating blood. We measured plasma levels of plasmin-alpha 2-plasmin inhibitor complex, fibrinogen degradation products (FgDP) and fibrin degradation products (FbDP) following desmopressin infusion in 19 patients with bleeding disorders or thrombophilia. Administration of desmopressin (0.3-0.4 microgram/kg) produced a 4.0-fold increase in plasmin-alpha 2-plasmin inhibitor complex at 30 min, whereas neither FgDP nor FbDP was elevated significantly. These findings indicate that desmopressin infusion provokes the generation of plasmin in vivo, but most of the plasmin generated is complexed to alpha 2-plasmin inhibitor and does not degradate fibrin or fibrinogen.
已知醋酸去氨加压素(DDAVP)可刺激内皮细胞释放组织型纤溶酶原激活物(t-PA),但尚不清楚循环血液中t-PA的增加是否真的能引发纤溶酶生成及纤维蛋白(原)溶解。我们测定了19例出血性疾病或易栓症患者输注去氨加压素后血浆中纤溶酶-α2-纤溶酶抑制物复合物、纤维蛋白原降解产物(FgDP)和纤维蛋白降解产物(FbDP)的水平。输注去氨加压素(0.3 - 0.4微克/千克)后30分钟,纤溶酶-α2-纤溶酶抑制物复合物增加了4.0倍,而FgDP和FbDP均未显著升高。这些发现表明,输注去氨加压素可在体内引发纤溶酶生成,但生成的大部分纤溶酶与α2-纤溶酶抑制物结合,并不降解纤维蛋白或纤维蛋白原。