Journal of Applied Physiology, Vol 63, Issue 3 1262-1267, Copyright © 1987 by American Physiological Society
Operation Everest II: coagulation system during prolonged decompression to 282 Torr
M. Andrew, H. O'Brodovich and J. Sutton
Department of Pediatrics, McMaster University Health Sciences Centre, Chedoke-McMaster Hospitals, Hamilton, Ontario, Canada.
Thromboembolic phenomena may occur as humans ascend to high altitude. To
investigate the role of the coagulation cascade and its inhibitors in these
disorders, venous blood was obtained from eight subjects who participated
in the Operation Everest II project. Samples were obtained before and 5 min
after completion of a progressive incremental exercise test to exhaustion
at sea level and atmospheric pressures of 380 (18,000 ft) and 282 Torr
(25,000 ft). Plasma was analyzed for the activity or concentration of
factors II, V, VII, VIII complex, IX-XIII, prekallikrein,
high-molecular-weight kininogen, fibrinogen, antithrombin III, alpha
2-macroglobulin, alpha 2-antiplasmin, C1-esterase inhibitor, alpha
1-antitrypsin, and protein C. Prolonged exposure to simulated high altitude
did not alter the concentration of any of the coagulation factors or
inhibitors. Exercise increased the circulating concentrations of the factor
VIII complex at sea level, 380, and 282 Torr. However, the increment was
less at the simulated high altitudes. The increase in the factor VIII
complex was inversely related to arterial O2 saturation and directly
related to the work load achieved and blood pH and plasma lactate
concentrations. These studies suggest that the gradual development of
marked chronic hypoxia does not affect the coagulation cascade.
