Authors: Hodkinson P.D.¹; Hunt B.J.²; Parmar K.²; Ernsting J.¹

Source: Journal of Thrombosis and Haemostasis, Volume 1, Number 10, October 2003 , pp. 2131-2133(3)

Publisher: Wiley-Blackwell

Abstract:

Summary.

Background: Modern air travel entails a cabin altitude between 1520 and 2440 m (5000–8000 ft) and thus exposure to mild hypoxia. There is debate as to whether hypoxia is causally related to venous thromboembolism (VTE) occurring during or after travel. One study suggested that a short period of hypobaric hypoxia causes activation of coagulation. Objectives: To test the hypothesis that hypoxia alone (normobaric hypoxia) causes activation of coagulation, possibly through endothelial cell activation. Methods: Six healthy male volunteers were exposed for 3 h, while seated, on two separate occasions to (i) dry air (control) and (ii) hypoxic gas mixture (12.8% O₂ in N₂, equivalent to breathing air at 3660 m [12000 ft]). Results: There were no differences in hemostatic or endothelial markers between control and hypoxic groups, but platelet and leukocyte counts increased and were significantly higher in the hypoxic group. There were increases in fibrinogen and von Willebrand factor, as well as rheological changes, but these were not significantly different between control and hypoxic groups. Conclusions: This small study does not support the previous suggestion that hypoxia causes activation of coagulation, and suggests that immobility-induced rheological changes may be more significant in the etiology of VTE occurring during or after travel.

Keywords: hypoxia; risk; venous thromboembolism

Document Type: Research article

DOI: http://dx.doi.org/10.1046/j.1538-7836.2003.00407.x

Affiliations: 1: Division of Physiology, GKT School of Biomedical Sciences; and 2: Thrombosis and Vascular Biology Group, Department of of Haematology, St Thomas'. Hospital, UK

Publication date: 2003-10-01

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