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静脉血栓栓塞症的病理生理学

Pathophysiology of venous thromboembolism.

作者信息

Nielsen H K

机构信息

Cardiology Department, Skejby Hospital, University of Aarhus, Denmark.

出版信息

Semin Thromb Hemost. 1991;17 Suppl 3:250-3.

PMID:1754882
Abstract

Venous thromboembolism is complex with a multifactorial etiology. The Virchow triad (changes in blood flow, changes in vessel wall, and changes in the properties of blood) gives the main factors involved in venous thromboembolism. Venous stasis during immobilization in general anesthesia, stroke with hemiparesis, and heart failure plays a central role. The thromboembolic process can be initiated by a disturbance in the normal "hemostatic balance," with an increased thrombogenic potential, due to release of thromboplastin and collagen exposure during vessel wall injury by stasis and hypoxia, decreased fibrinolysis during surgery, malignancy, among others. Many substances modify these processes, including heparan sulfate, AT III, protein C, t-PA inhibitor, and alpha 2-antiplasmin.

摘要

静脉血栓栓塞症病因复杂,涉及多种因素。魏尔啸三联征(血流改变、血管壁改变和血液性质改变)给出了静脉血栓栓塞症的主要相关因素。全身麻醉下制动、偏瘫性中风和心力衰竭期间的静脉淤滞起着核心作用。血栓栓塞过程可由正常“止血平衡”的紊乱引发,由于淤滞和缺氧导致血管壁损伤时组织凝血活酶释放和胶原暴露,手术、恶性肿瘤等期间纤维蛋白溶解减少,从而使血栓形成潜能增加。许多物质会改变这些过程,包括硫酸乙酰肝素、抗凝血酶III、蛋白C、组织型纤溶酶原激活物抑制剂和α2-抗纤溶酶。

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