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Stenosis of the Inferior Vena Cava: A Murine Model of Deep Vein Thrombosis
Published on: December 22, 2017
Is mild normobaric hypoxia a risk factor for venous thromboembolism?
P D Hodkinson1, B J Hunt, K Parmar
1Division of Physiology, GKT School of Biomedical Sciences, St Thomas'. Hospital, Guy's and St. Thomas' Trust, London SE1 7EH, UK.
Journal of Thrombosis and Haemostasis : JTH
|October 3, 2003
Summary
This study found that hypoxia alone does not activate coagulation. Immobility may be a more significant factor in travel-related venous thromboembolism (VTE).
Area of Science:
- Aerospace Medicine
- Physiology
- Hematology
Background:
- Air travel exposes passengers to cabin altitudes (1520-2440 m), causing mild hypoxia.
- The link between hypoxia and venous thromboembolism (VTE) during or after flights is debated.
- Previous research suggested hypobaric hypoxia activates coagulation.
Purpose of the Study:
- To investigate if normobaric hypoxia alone activates coagulation.
- To determine if hypoxia induces endothelial cell activation.
Main Methods:
- Six healthy males were exposed to normobaric hypoxia (12.8% O2, equivalent to 3660 m) for 3 hours.
- Participants were seated during exposure.
- Hemostatic, endothelial, platelet, and leukocyte markers were measured.
Main Results:
- No significant differences in hemostatic or endothelial markers were observed between hypoxia and control conditions.
- Platelet and leukocyte counts were significantly higher in the hypoxia group.
- Increases in fibrinogen and von Willebrand factor showed no significant difference between groups.
Conclusions:
- The study does not support the hypothesis that hypoxia alone activates coagulation.
- Immobility-induced rheological changes may play a more significant role in VTE etiology during air travel.
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