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肺栓塞中的凝血与血管壁。

Coagulation and the vessel wall in pulmonary embolism.

机构信息

Department of Internal Medicine II, Division of Cardiology, Medical University of Vienna, Vienna, Austria.

出版信息

Pulm Circ. 2013 Dec;3(4):728-38. doi: 10.1086/674768.

DOI:10.1086/674768
PMID:25006391
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4070824/
Abstract

Venous thromboembolism comprises deep-vein thrombosis, thrombus in transit, acute pulmonary embolism, and chronic thromboembolic pulmonary hypertension (CTEPH). Pulmonary thromboemboli commonly resolve, with restoration of normal pulmonary hemodynamics. When they fail to resorb, permanent occlusion of the deep veins and/or CTEPH are the consequences. Apart from endogenous fibrinolysis, venous thrombi resolve by a process of mechanical fragmentation, through organization of the thromboembolus by invasion of endothelial cells, leukocytes, and fibroblasts leading to recanalization. Recent data utilizing various models have contributed to a better understanding of venous thrombosis and the resolution process that is directed at maintaining vascular patency. This review summarizes the plasmatic and cellular components of venous thrombus formation and resolution.

摘要

静脉血栓栓塞症包括深静脉血栓形成、移行性血栓、急性肺栓塞和慢性血栓栓塞性肺动脉高压(CTEPH)。肺血栓栓子通常可溶解,恢复正常的肺血流动力学。如果不能溶解,深静脉永久性闭塞和/或 CTEPH 则是后果。除了内源性纤维蛋白溶解外,静脉血栓通过机械碎裂的过程溶解,通过内皮细胞、白细胞和成纤维细胞的入侵使血栓栓子发生组织化,从而导致再通。最近利用各种模型的研究数据有助于更好地理解静脉血栓形成和溶解过程,该过程旨在维持血管通畅。本综述总结了静脉血栓形成和溶解的血浆和细胞成分。

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Nucleic acid scavengers inhibit thrombosis without increasing bleeding.核酸清除剂抑制血栓形成而不增加出血。
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