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. 1967 Dec;46(12):1986–1998. doi: 10.1172/JCI105688

Carbon Monoxide Production Associated with Ineffective Erythropoiesis*

Peter White 1,2,, Ronald F Coburn 1,2,§, William J Williams 1,2,ǁ, Manfred I Goldwein 1,2, Mary L Rother 1,2, Brenda C Shafer 1,2
PMCID: PMC292951  PMID: 6074003

Abstract

The rate of endogenous carbon monoxide production (˙Vco), determined by the closed rebreathing system technique, was elevated above the normal range in four of five patients studied with ineffective erythropoiesis (four patients with primary refractory anemia, one with thalassemia). The mean molar ratio of ˙Vco to ˙Vheme (rate of circulating heme catabolism, determined from 51Cr red cell survival curves) was 3.0 ± 0.6 (SE), indicating that most of the CO originated from sources other than circulating erythrocyte hemoglobin, in contrast to previous findings in patients with hemolytic anemia, where ˙Vco paralleled ˙Vheme closely.

After administration of glycine-2-14C to these patients, endogenous CO was isolated by washout of body CO stores at high pO2 or by reacting peripheral venous blood samples with ferricyanide. The CO was then oxidized to CO2 by palladium chloride and trapped for counting in a liquid scintillation spectrometer. “Early labeled” peaks of 14CO were demonstrated which paralleled “early labeled” peaks of stercobilin and preceded maximal labeling of circulating heme. Production of “early labeled” 14CO in patients with ineffective erythropoiesis was greatly increased, up to 14 times that found in a normal subject.

The increased ˙Vco and “early 14CO” production shown by these patients are presumably related mainly to heme catabolism in the marrow. The possibility exists that hepatic heme and porphyrin compounds may also contribute significantly to ˙Vco, as suggested by the finding of a high ˙Vco in an additional patient with porphyria cutanea tarda.

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1986

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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