Orthostatic Hypercoagulability: A Novel Physiological Mechanism to Activate the Coagulation System

Orthostatic stress causes significant plasma shift and raises transmural pressure in lower extremities, resulting in an increase in endothelial activation and plasma proteins concentrations, possibly including coagulation factors. This may lead to activation of the coagulation system during standing...

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Bibliographic Details
Published in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 2008-06, Vol.51 (6), p.1545-1551
Main Authors: Masoud, Muhannad, Sarig, Galit, Brenner, Benjamin, Jacob, Giris
Format: Article
Language:English
Subjects:
Adult
Arterial hypertension. Arterial hypotension
Biological and medical sciences
Blood and lymphatic vessels
Blood Coagulation - physiology
Blood Pressure - physiology
Cardiology. Vascular system
Endocrine kidney. Renin-angiotensin-aldosterone system
Endothelium, Vascular - physiology
Factor V - metabolism
Factor VIII - metabolism
Female
Fibrinogen - metabolism
Fundamental and applied biological sciences. Psychology
Hematocrit
Humans
Male
Medical sciences
Peptide Fragments - metabolism
Plasma Volume - physiology
Posture
Protein C - metabolism
Protein Precursors - metabolism
Prothrombin - metabolism
Thrombophilia - physiopathology
Thromboplastin - metabolism
Venous Thromboembolism - physiopathology
Vertebrates: endocrinology
von Willebrand Factor - metabolism
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Summary:Orthostatic stress causes significant plasma shift and raises transmural pressure in lower extremities, resulting in an increase in endothelial activation and plasma proteins concentrations, possibly including coagulation factors. This may lead to activation of the coagulation system during standing. To test this hypothesis, we recruited 18 healthy volunteers (9 females and 9 males; mean age25±1.2 years; body mass index21.7±0.5 kg/m). Hemodynamics, plasma shift (extrapolated from sequential hematocrit concentration), plasma proteins, and coagulation tests, including procoagulants; fibrinogen, factor V, and factor VIII activity; prothrombin fragments 1 and 2; and endothelial activation–related factors (tissue factor and von Willebrand factor), as well as protein C global pathway, were determined at rest supine and at 15 minutes, 30 minutes, and 60 minutes of still standing. Thirty minutes of standing caused a decrease in plasma volume by 12.0±0.5% and an increase in plasma protein by 13.0±0.7%. Fibrinogen, factor V, and factor VIII activity rose by 12.0±1.2%, 13.0±1.0%, and 40.0±6.0% (P
ISSN:0194-911X
1524-4563
DOI:10.1161/HYPERTENSIONAHA.108.112003