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Research Article Free access | 10.1172/JCI105835

Maximal erythrocyte and hemoglobin catabolism

Ronald F. Coburn and Peter B. Kane

Department of Physiology (Graduate Division), School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104

Department of Medicine, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104

Find articles by Coburn, R. in: PubMed | Google Scholar

Department of Physiology (Graduate Division), School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104

Department of Medicine, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104

Find articles by Kane, P. in: PubMed | Google Scholar

Published June 1, 1968 - More info

Published in Volume 47, Issue 6 on June 1, 1968
J Clin Invest. 1968;47(6):1435–1446. https://doi.org/10.1172/JCI105835.
© 1968 The American Society for Clinical Investigation
Published June 1, 1968 - Version history
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Abstract

A series of experiments were performed on anesthetized dogs in which varying quantities of normal canine erythrocytes damaged by incubation with N-ethylmaleimide were injected into the circulation. Cell sequestration and catabolism of hemoglobin to carbon monoxide remained normal after injections that contained from 0.058 to 0.154 g of hemoglobin per kg of body weight.

After administration of larger quantities of these cells, from 0.154 to 0.364 g of hemoglobin per kg of body weight, sequestration remained normal but the rate of catabolism of hemoglobin to carbon monoxide reached a maximum. Large quantities of hemoglobin entered the plasma in these experiments at a time when cell sequestration in the reticuloendothelial system appeared to be virtually complete. After injection of even larger quantities of damaged erythrocytes, 0.545 and 0.552 g of hemoglobin per kg, sequestration became slightly delayed, but was complete.

These data appear to indicate that (a) the maximal rate of hemoglobin catabolism in normal anesthetized dogs averages approximately 0.07 g/kg of body weight per hr; (b) hemoglobinemia can result from “overloading” the reticuloendothelial system with damaged sequestered cells and, therefore, may not always indicate “intravascular” hemolysis; and (c) the sequestering function of the reticuloendothelial system appears not to limit the maximal rate of catabolism of hemoglobin. The limiting parameter or parameters were not defined in these studies.

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