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首页> 外文期刊>Annals of Biomedical Engineering: The Journal of the Biomedical Engineering Society >Computational Model for Hyperfibrinolytic Onset of Acute Traumatic Coagulopathy
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Computational Model for Hyperfibrinolytic Onset of Acute Traumatic Coagulopathy

机译:急性创伤性凝血病的高纤维蛋白溶解术衰退的计算模型

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摘要

The onset of acute traumatic coagulopathy in trauma patients exacerbates hemorrhaging and dramatically increases mortality. The disease is characterized by increased localized bleeding, and the mechanism for its onset is not yet known. We propose that the fibrinolytic response, specifically the release of tissue-plasminogen activator (t-PA), within vessels of different sizes leads to a variable susceptibility to local coagulopathy through hyperfibrinolysis which can explain many of the clinical observations in the early stages from severely injured coagulopathic patients. We use a partial differential equation model to examine the consequences of vessel geometry and extent of injury on fibrinolysis profiles. In addition, we simulate the efficacy of tranexamic acid treatment on coagulopathy initiated through endothelial t-PA release, and are able to reproduce the time-sensitive nature of the efficacy of this treatment as observed in clinical studies.
机译:创伤患者急性创伤凝血病的发病加剧了出血,显着提高了死亡率。 该疾病的特征在于局部出血增加,并且其发作的机制尚不清楚。 我们提出纤维蛋白溶解反应,特别是释放组织 - 纤溶酶原激活剂(T-PA),不同尺寸的血管内通过高纤维蛋白溶解的局部凝血病变可变易感性,其可以在严重的阶段解释许多临床观察 受伤的凝血患者。 我们使用局部微分方程模型来检查血管几何形状和损伤程度对纤维蛋白溶解型材的后果。 此外,我们模拟促进宁酸处理对通过内皮T-PA释放引发的凝血病的疗效,并且能够在临床研究中观察到的这种处理的功效的时间敏感性。

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