Formation of fibrin monomers in experimental disseminated intravascular coagulation and its inhibition by recombinant hirudin.

Circulatory shock Pub Date : 1994-04-01
G Dickneite, J Czech, H Keuper
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Abstract

An experimental disseminated intravascular coagulation (DIC) was induced in female CD rats by the intravenous administration of living bacteria (9.5 x 10(7) cfu Klebsiella pneumoniae), sublethal (5 mg/kg) or lethal (50 mg/kg) lipopolysaccharide (LPS), or tissue factor (1.5 micrograms/kg i.v. bolus or 0.4 micrograms/kg x hr i.v. infusion). We used a new fibrin monomer (FM) assay to follow the course of DIC. FM were detected by their ability to stimulate the tissue-type (t-PA) plasminogen activator dependent conversion of plasminogen to plasmin by a chromogenic assay. Miniplasminogen was used instead of plasminogen to avoid interference of the assay by alpha 2-antiplasmin. As a marker of DIC, elevated levels of FM were observed with all DIC-inducing agents (plasma levels were up to 90 micrograms/ml). The kinetics of FM formation were similar to the course of thrombin-antithrombin III (TAT) levels (maximal plasma levels 70 ng/ml); however, in the bacterial infection group, both parameters rose after a lag phase of about 1 hr. A 4 hr infusion of the highly specific thrombin inhibitor recombinant (rec.) hirudin (0.125 mg/kg x hr) resulted in a decrease of FM levels from 89.2 +/- 14.4 micrograms/ml in the LPS group (n = 10) to 27.4 +/- 11.2 micrograms/ml in the rec. hirudin group (n = 10; P < 0.001). The respective values for TAT levels were 73.1 +/- 19.7 micrograms/ml in the LPS group and 52.7 +/- 15.7 ng/ml in the rec. hirudin group (P < 0.001). Other coagulation parameters, such as platelets, fibrinogen, and fibrin(ogen) degradation products, were ameliorated accordingly.(ABSTRACT TRUNCATED AT 250 WORDS)

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实验性弥散性血管内凝血中纤维蛋白单体的形成及其重组水蛭素的抑制作用。
雌性CD大鼠通过静脉注射活细菌(9.5 × 10(7) cfu肺炎克雷伯菌)、亚致死(5 mg/kg)或致死(50 mg/kg)脂多糖(LPS)或组织因子(1.5微克/kg静脉滴注或0.4微克/kg静脉滴注)诱导实验性弥散性血管内凝血(DIC)。我们采用一种新的纤维蛋白单体(FM)测定方法来跟踪DIC的病程。通过显色试验,通过其刺激组织型(t-PA)纤溶酶原激活剂依赖的纤溶酶原向纤溶酶转化的能力来检测FM。用微纤溶酶原代替纤溶酶原,避免了α - 2抗纤溶酶对测定的干扰。作为DIC的标志物,所有DIC诱导剂均可观察到FM水平升高(血浆水平高达90微克/毫升)。FM形成的动力学与凝血酶-抗凝血酶III (TAT)水平的过程相似(最大血浆水平为70 ng/ml);然而,在细菌感染组,这两个参数在大约1小时的滞后期后上升。高特异性凝血酶抑制剂重组水蛭素(0.125 mg/kg x hr)输注4小时,导致FM水平从LPS组(n = 10)的89.2 +/- 14.4微克/ml降至水蛭素组(n = 10)的27.4 +/- 11.2微克/ml;P < 0.001)。LPS组TAT值为73.1 +/- 19.7 μ g/ml,水蛭素组TAT值为52.7 +/- 15.7 μ g/ml (P < 0.001)。其他凝血参数,如血小板、纤维蛋白原和纤维蛋白(原)降解产物,也相应改善。(摘要删节250字)
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