Darius H, Grodzinska L, Hafner G, Meyer J
II. Medizinische Klinik und Poliklinik, Johannes Gutenberg-Universität, Mainz.
Z Kardiol. 1991;80 Suppl 5:47-50.
The influence of molsidomine on endogenous fibrinolytic activity was studied in a double-blind, randomized, placebo-controlled trial involving 12 male healthy volunteers. When measured 3 h after oral intake of molsidomine (16 mg, slow-release formulation) the activity of tissue plasminogen activator (t-PA) in plasma was significantly increased from 1.1 +/- 0.1 to 1.6 +/- 0.1 IU/ml. In contrast, the activity of plasminogen activator inhibitor (PAI-I) decreased from 17 +/- 2 to 12 +/- 1 AU/ml. The ratio of t-PA/PAI-I (x 100), calculated as index for the endogenous fibrinolytic activity increased significantly from 8.1 +/- 1.1 to 14.5 +/- 1.6. The ratio was unaltered after intake of placebo. Additionally, collagen-induced platelet aggregation was significantly inhibited following intake of molsidomine. The results demonstrate a significant increase in endogenous fibrinolytic activity after oral intake of molsidomine. These effects may be of therapeutic value in patients with coronary heart disease and unstable angina.
在一项涉及12名男性健康志愿者的双盲、随机、安慰剂对照试验中,研究了吗多明对内源性纤溶活性的影响。口服吗多明(16毫克,缓释制剂)3小时后测量,血浆中组织纤溶酶原激活物(t-PA)的活性从1.1±0.1显著增加至1.6±0.1国际单位/毫升。相比之下,纤溶酶原激活物抑制剂(PAI-I)的活性从17±2降至12±1任意单位/毫升。作为内源性纤溶活性指标计算的t-PA/PAI-I比值(×100)从8.1±1.1显著增加至14.5±1.6。服用安慰剂后该比值未改变。此外,服用吗多明后胶原诱导的血小板聚集受到显著抑制。结果表明口服吗多明后内源性纤溶活性显著增加。这些作用可能对冠心病和不稳定型心绞痛患者具有治疗价值。