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组织型纤溶酶原激活剂(Tissue-type plasminog-cn activator简称t-pA)是一种天然的、能选择性溶解血凝块而不引起全身纤溶状态的物质。它与纤维蛋白有较强的亲和力,在血中形成t-pA纤维蛋白复合物,纤溶酶原与该复合物结合,停留在血凝块表面,转变为纤溶酶。作者从黑色素瘤组织培养上清液中分离出人体t-pA,给有冠状动脉血栓的狗作静脉注射,血栓溶解迅速出现而不伴有血中纤维蛋白原和纤溶醇原减少,纤维蛋白原降解产物积聚或α_2以抗纤溶酶耗失等全身纤溶现象。在颈静脉血栓或肺梗塞的兔作活体试验,也证实t-pA有溶解血块的作用。本文报告了用t-pA治疗7例心肌梗塞患者,年龄51～68岁,包括5例左前降支及2例右冠状动脉阻塞。用药途径为冠状动脉内和静脉内滴注,剂量为6.0×10~5至1.4×0~^lu,30～60分钟滴完,其中2例加用链激酶250,000Iu对比疗效。7例病人输注t-pA后,6例在19～50分钟内血栓溶解,静脉及冠状动脉用药均成
Tissue-type plasminogen activator (t-pA) is a natural substance that selectively dissolves blood clots without causing systemic fibrinolysis. It has a strong affinity with fibrin in the blood to form t-pA fibrin compound, plasminogen and the complex binding, stay in the blood clot surface, into plasmin. The authors isolated human t-pA from melanoma tissue culture supernatants and injected intravenously into dogs with coronary artery thrombosis. Thrombolysis quickly appeared without a decrease in blood fibrinogen and fibrinolysis. Fibrin The original degradation product accumulation or α_2 anti-fibrinolysis and other systemic fibrinolysis phenomenon. In vivo tests of jugular vein thrombosis or pulmonary infarction in rabbits also confirmed the role of t-pA in clotting. This paper reports 7 patients with myocardial infarction treated with t-pA, aged 51-68 years, including 5 cases of left anterior descending coronary artery and 2 cases of right coronary artery obstruction. The route of administration for intracoronary and intravenous infusion, the dose of 6.0 × 10 ~ 5 to 1.4 × 0 ~ lu, 30 to 60 minutes drops, of which 2 cases with streptokinase 250,000Iu contrast effect. Thrombolysis occurred in 6 to 19 patients within 7 to 50 minutes after infusion of t-pA in 7 patients. Both intravenous and coronary drug administration