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首页> 外文期刊>Thrombosis Research: An International Journal on Vascular Obstruction, Hemorrhage and Hemostasis >Effect of some new thioglycosides on endotoxin-induced disseminated intravascular coagulation in rabbits.
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Effect of some new thioglycosides on endotoxin-induced disseminated intravascular coagulation in rabbits.

机译：一些新的硫代糖苷对内毒素诱导的兔弥散性血管内凝血的影响。

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Disseminated intravascular coagulation (DIC) is a systemic thrombohemorrhagic disorder seen in association with many clinical situations, e.g. sepsis, malignancy, obstetrical complications and intravascular hemolysis. In our model, disseminated intravascular coagulation was induced in rabbits by two consecutive intravenous bolus injections of endotoxin from Escherichia coli, 80 and 40 microg/kg. The control group was treated with 0.9% saline. The activity of thioglycosides was compared to unfractionated heparin (UFH) and efegatran with and without administration of endotoxin. Drugs were administered in the following doses: heparin 50 and 100 IU/kg/h i.v. infusion; efegatran 0.25 and 0.5 mg/kg/h i.v. infusion; GYKI 39521 (RGH-1875) as well as GYKI 39541 (RGH-1962) 12.5 and 25 mg/kg per os. Thioglycosides did not modify coagulation parameters in this model [prothrombin time (PT), activated partial thromboplastin time (APTT), thrombin time (TT)] as compared with endotoxin/vehicle group. The changes in TFPI level after administration of thioglycosides and heparin were similar in the mentioned model to those without endotoxin. Endotoxin-induced changes of leukocyte count were not affected by GYKI 39521 and GYKI 39541 treatment in our model. Diminution of fibrinogen level and platelet count was prevented by GYKI 39521 and GYKI 39541. Fibrin degradation products and fibrinolysis were significantly decreased by GYKI 39521 and GYKI 39541. The thioglycosides may have a lower risk of bleeding in the treatment of disseminated intravascular coagulation than heparin.
机译：弥散性血管内凝血（DIC）是一种全身性血栓出血性疾病，与许多临床情况相关，例如败血症，恶性肿瘤，产科并发症和血管内溶血。在我们的模型中，通过连续两次静脉推注大肠埃希氏菌内毒素，分别为80和40微克/千克，在兔中诱导了弥散性血管内凝血。对照组用0.9％生理盐水治疗。将硫代糖苷的活性与未施用内毒素的普通肝素（UFH）和efegatran进行了比较。药物按以下剂量给药：肝素50和100 IU / kg / h静脉内。输液静脉注射efegatran 0.25和0.5 mg / kg / h输液GYKI 39521（RGH-1875）和GYKI 39541（RGH-1962）12.5和25 mg / kg / os。与内毒素/载体组相比，硫糖苷在该模型中没有改变凝血参数[凝血酶原时间（PT），活化的部分凝血活酶时间（APTT），凝血酶时间（TT）]。在上述模型中，硫代糖苷和肝素给药后TFPI水平的变化与无内毒素的相似。在我们的模型中，内毒素诱导的白细胞计数变化不受GYKI 39521和GYKI 39541处理的影响。 GYKI 39521和GYKI 39541防止了纤维蛋白原水平和血小板数量的减少。GYKI39521和GYKI 39541显着降低了纤维蛋白的降解产物和纤维蛋白溶解。硫代糖苷在治疗弥散性血管内凝血方面的出血风险可能比肝素低。

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