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[缺氧与止血的相互作用——缺氧是高原地区的促血栓形成因素?]

[Interaction of hypoxia and haemostasis--hypoxia as a prothrombotic factor at high altitude?].

作者信息

Schobersberger Wolfgang, Hoffmann Georg, Gunga Hanns-Christian

机构信息

Institut für Urlaubs-, Reise- und Höhenmedizin, Private Universität für Gesundheitswissenschaften, Medizinische Informatik und Technik, Tirol, Hall i. Tirol, Osterreich.

出版信息

Wien Med Wochenschr. 2005 Apr;155(7-8):157-62. doi: 10.1007/s10354-005-0163-7.

Abstract

For an extended period of time various research projects have been conducted on the relationship of hypoxia and haemostasis. The enclosed article contains the conclusion to which extent lack of oxygen can activate the coagulation system and induce a prothrombotic state. The majority of studies proved a shortening of coagulation times during acute exposure to hypoxia, whereas activated parameters of coagulation and fibrinolysis like prothrombin fragment F1+2 as well as thrombin-antithrombin III complexes and D-dimer remained mostly unmodified. It is suggested that a prolonged sojourn at high altitudes could lead to activation of the coagulation system through an increase of haematocrit and blood viscosity. Recently it was proven that people living at high altitudes show an enhanced risk of stroke incidents. The significance of the change in haemostasis on that outcome has not yet been part of the research. However, it has been proven that the activity of the coagulation system does not play a pathophysiological part in the development of acute mountain sickness and high altitude pulmonary edema. Recent studies also demonstrated that moderate hypoxia during long haul flights may not be the main trigger in inducing deep vein thrombosis in passengers.

摘要

长期以来,人们针对缺氧与止血之间的关系开展了各类研究项目。随附文章给出了关于缺氧能在多大程度上激活凝血系统并诱发血栓前状态的结论。大多数研究证明,急性缺氧时凝血时间会缩短,而凝血和纤维蛋白溶解的激活参数,如凝血酶原片段F1+2、凝血酶-抗凝血酶III复合物以及D-二聚体大多未发生改变。有人提出,在高海拔地区长期停留可能会通过增加血细胞比容和血液粘度导致凝血系统激活。最近有证据表明,生活在高海拔地区的人中风风险增加。止血变化对该结果的影响尚未成为研究内容。然而,已经证明凝血系统的活性在急性高山病和高原肺水肿的发展过程中不发挥病理生理作用。最近的研究还表明,长途飞行期间的中度缺氧可能不是诱发乘客深静脉血栓形成的主要触发因素。

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