Samama M, Verdy E, Conard J, Vahanian A, Michel P, Van Dreden P, Nguyen G, Horellou M H, Combrisson A, Acar J
Arch Mal Coeur Vaiss. 1986 Oct;79(11):1618-24.
A group of 37 patients with myocardial infarction less than 6 hours old was given 5,000 IU of heparin and 0.75 mg/kg of tissue plasminogen activator (rt-PA) (Group A, N = 18) or placebo (Group B, N = 19) intravenously over 90 minutes in a double blind study. Blood sampling was performed before, during and after treatment. The plasma rt-PA concentrations (micrograms/ml) of Group A were as follows: (Table: see text) The concentrations of plasminogen and antiplasmin have decreased significantly as did the fibrinogen level: a concentration of 1 g/l was observed in 7 cases during rt-PA therapy, lasting for 4 to 8 hours after the end of the infusion of rt-PA in 3 cases. The increase of FDP during rt-PA (m = 551 and 222 micrograms/ml at the 60th and 90th minutes) was relatively moderate considering the average level of defibrination (61%). No significant biological changes were observed in Group B. These results support those of our in vitro trials: at comparable thrombolytic activities, the reduction of plasma fibrinogen is less with rt-PA than with streptokinase (SK) or urokinase (UK). However, at concentrations 1 microgram/ml, rt-PA causes almost complete defibrination.
在一项双盲研究中，一组37例心肌梗死发病时间小于6小时的患者在90分钟内静脉给予5000国际单位肝素和0.75毫克/千克组织型纤溶酶原激活剂（rt-PA）（A组，N = 18）或安慰剂（B组，N = 19）。在治疗前、治疗期间和治疗后进行血样采集。A组的血浆rt-PA浓度（微克/毫升）如下：（表格：见正文）纤溶酶原和抗纤溶酶的浓度以及纤维蛋白原水平均显著下降：在rt-PA治疗期间，7例患者纤维蛋白原浓度降至1克/升，3例患者在rt-PA输注结束后持续4至8小时。考虑到平均纤维蛋白溶解水平（61%），rt-PA治疗期间FDP的增加（第60分钟和第90分钟时分别为551和222微克/毫升）相对适中。B组未观察到明显的生物学变化。这些结果支持我们的体外试验结果：在溶栓活性相当的情况下，rt-PA导致的血浆纤维蛋白原减少比链激酶（SK）或尿激酶（UK）少。然而，在浓度为1微克/毫升时，rt-PA几乎可导致完全纤维蛋白溶解。
