Unaltered blood coagulation and platelet function in healthy subjects exposed to acute hypoxia

Acute hypoxia has been suspected to cause blood coagulation and platelet activation. Our aim was to study blood coagulation and platelet function during a short hypoxic exposure.

Healthy nonsmoking men (N = 10) inhaled a normobaric hypoxic gas mixture containing 8% of oxygen (92% nitrogen) for 7 min via a face mask. Venous blood was collected 5 min before and during the 5 to 7 min of hypoxia exposure (i.e., pretest and hypoxia samples, respectively) while monitoring arterial oxygen saturation (SaO2) with pulse oximetry. Blood sampling was completed in 2 min and the face mask was removed. Venous epinephrine and norepinephrine, complete blood counts, and a panel of coagulation markers were analyzed. Platelet aggregation induced by ristocetin, adenosine diphosphate (ADP), arachidonic acid, and thrombin receptor activating peptide was studied with Multiplate and shear force-dependent functions with PFA-100R (collagen/epinephrine and collagen/ADP cartridges), both assays in whole blood.

During hypoxia, SaO2 declined from 98 to 58% (ranges 97-99% vs. 42-85%), while heart rate increased from 69/min to 94/min (SD 11 vs. SD 13). Venous epinephrine and norepinephrine levels also increased. This short hypoxia induced minor but uniform increases in red cells, reticulocytes, and leukocytes and decreases in platelet counts. Plateletfunctions and prothrombin time, APTT, thrombin time, D-dimer, fibrinogen levels or von Willebrand factor (VWF), antithrombin, factor V (FV) or FVIII activities did not change.

Profound acute hypoxia failed to affect blood coagulation or platelet functions in healthy individuals.