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October 1974

Oxygen Transport in Hemoglobin Köln: Effect of Increased Oxygen Affinity in Absence of Compensatory Erythrocytosis

Author Affiliations

From the departments of medicine, laboratory medicine, and physiology and biophysics, University of Washington School of Medicine, Seattle. Dr. Lenfant is now with the National Heart and Lung Institute, Bethesda, Md; and Dr. Woodson is now with the University of Wisconsin School of Medicine, Madison.

Arch Intern Med. 1974;134(4):711-715. doi:10.1001/archinte.1974.00320220113014

Oxygen transport was evaluated in patients with hemoglobin Köln. This hemoglobinopathy is characterized by an increased rate of destruction of red blood cells (RBC), a loss of heme groups from intracellular hemoglobin of surviving RBC, and an impairment of oxygen release from hemoglobin. Hemoglobin concentration, cardiac output, and oxygen consumption were essentially normal. Mixed venous oxygen tension was decreased, averaging 30 mm Hg. Renal blood flow was reduced by one third to one half. Evidence of latent hypoxia and decreased reserve were suggested by increased erythropoietin, decreased mean end capillary oxygen pressure, and evidence of blood flow redistribution. While essentially asymptomatic at rest and with ordinary activity, the subjects are probably more vulnerable than normal persons to diseases that would further impair oxygen delivery.

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