Normal arterial blood at sea level unloads only about 22% of its oxygen to the tissues at rest; the percent saturation is reduced from 97% in arterial blood to 75% in venous blood. As a partial compensation for the decrease in oxygen content at high altitude, the affinity of hemoglobin for oxygen is reduced, so that a higher proportion of oxygen is unloaded. This occurs because the low oxyhemoglobin content of red blood cells stimulates the production of 2,3-DPG, which in turn decreases the affinity of hemoglobin for oxygen.
The action of 2,3-DPG to decrease the affinity of hemoglobin for oxygen thus predominates over the action of respiratory alkalosis (caused by the hyperventilation) to increase the affinity. At very high altitudes, however, the story becomes more complex. In one study, the very low arterial PO2 (28 mmHg) of subjects at the summit of Mount Everest stimulated intense hyperventilation, so that the arterial PCO2 was decreased to 7.5 mmHg. The resultant respiratory alkalosis (in this case, arterial pH greater than 7.7) caused the oxyhemoglobin dissociation curve to shift to the left (indicating greater affinity of hemoglobin for oxygen) despite the antagonistic effect of increased 2,3-DPG concentrations. It was suggested that the increased affinity of hemoglobin for oxygen caused by the respiratory al-kalosis may have been beneficial at such a high altitude, since it increased the loading of hemoglobin with oxygen in the lungs.
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