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Research Article Free access | 10.1172/JCI105875

Improved oxygen release: an adaptation of mature red cells to hypoxia

Miles J. Edwards, Miles J. Novy, Carrie-Lou Walters, and James Metcalfe

1Heart Research Laboratory and Division of Chest Diseases, Department of Medicine, University of Oregon Medical School, Portland, Oregon 97201

Find articles by Edwards, M. in: PubMed | Google Scholar

1Heart Research Laboratory and Division of Chest Diseases, Department of Medicine, University of Oregon Medical School, Portland, Oregon 97201

Find articles by Novy, M. in: PubMed | Google Scholar

1Heart Research Laboratory and Division of Chest Diseases, Department of Medicine, University of Oregon Medical School, Portland, Oregon 97201

Find articles by Walters, C. in: PubMed | Google Scholar

1Heart Research Laboratory and Division of Chest Diseases, Department of Medicine, University of Oregon Medical School, Portland, Oregon 97201

Find articles by Metcalfe, J. in: PubMed | Google Scholar

Published August 1, 1968 - More info

Published in Volume 47, Issue 8 on August 1, 1968
J Clin Invest. 1968;47(8):1851–1857. https://doi.org/10.1172/JCI105875.
© 1968 The American Society for Clinical Investigation
Published August 1, 1968 - Version history
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Abstract

Blood from patients with erythrocytosis secondary to arterial hypoxemia due either to congenital heart disease or to chronic obstructive pulmonary disease was shown to have a decreased affinity for oxygen; the average oxygen pressure required to produce 50% saturation of hemoglobin with oxygen was 29.8 mm Hg (average normal, 26.3 mm Hg). Such a displacement of the blood oxygen equilibrium curve promotes the release of oxygen from blood to the tissues.

Studies were also performed upon blood from a man with complete erythrocyte aplasia who received all of his red cells by transfusion from presumably normal persons. With mild anemia (hematocrit, 28%), the affinity of his blood for oxygen was slightly diminished (an oxygen pressure of 27.0 mm Hg was required to produce 50% saturation of hemoglobin with oxygen). With severe anemia (hematocrit, 13.5%), however, his blood had a markedly decreased oxygen affinity (an oxygen pressure of 29.6 mm Hg was required to produce 50% saturation of hemoglobin with oxygen).

We conclude that patients with various conditions characterized by an impairment in the oxygen supply system to tissues respond with a diminished affinity of their blood for oxygen. Although the mechanism which brings about this adaptation is not known, the displacement of the oxygen equilibrium curve is associated with an increase in heme-heme interaction. The decrease in blood oxygen affinity need not occur during erythropoiesis, but may be imposed upon mature circulating red cells.

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