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Haemostasis at high altitude.

G Le Roux1, P Larmignat, M Marchal

  • 1ARPE, UFR Médecine, Bobigny, France.

International Journal of Sports Medicine
|October 1, 1992
PubMed
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Altitude hypoxia affects blood clotting. Acute exposure shows normal clotting but altered thromboxane and prostacyclin. Chronic hypoxia at high altitudes increases D-dimer, indicating coagulation activation and potential endothelial damage.

Area of Science:

  • Physiology
  • Altitude Medicine
  • Hematology

Background:

  • Hemostasis (blood clotting) is crucial for survival.
  • Altitude hypoxia presents unique physiological challenges.
  • Previous studies have explored hemostasis during acute hypoxia.

Purpose of the Study:

  • To investigate hemostatic changes during acute and chronic altitude hypoxia.
  • To assess coagulation and endothelial markers at extreme altitudes.

Main Methods:

  • Analysis of platelet count, aggregability, and bleeding time.
  • Measurement of thromboxane, prostacyclin, coagulation factors (including F. VIII), antithrombin III, and fibrinopeptide A.
  • Assessment of D-dimer and F. VIII R. Cof/F. VIII R. Ag ratio in chronic hypoxia.

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Main Results:

  • Acute hypoxia: normal platelet count, aggregability, bleeding time; increased thromboxane and prostacyclin; unchanged coagulation factors (except increased F. VIII); normal modified antithrombin III; increased fibrinopeptide A in pulmonary edema.
  • Chronic hypoxia (6542 m): significant increase in D-dimer (p < 0.001), suggesting coagulation activation.
  • Chronic hypoxia: decreased F. VIII R. Cof/F. VIII R. Ag ratio, indicating endothelial cell damage.

Conclusions:

  • Hemostasis exhibits distinct alterations in response to acute and chronic altitude hypoxia.
  • Chronic exposure to extreme altitude is associated with coagulation activation and endothelial dysfunction.