Abstract
The anemia associated with chronic inflammation results from failure of the erythroid marrow to increase its production sufficiently to compensate for a modest shortening of red cell survival. This defect in erythropoiesis was characterized by examining the quantitative relationship between EP production and erythropoietic response in rats with adjuvant-induced polyarthritis. EP production was measured my exposing rats to 0.5 atm. for 6, 9, 12, or 15 hours. The immediate post-hypoxic EP levels (assayed in post-hypoxic polycythemic mice and expressed as percent RBC 50Fe incorporation per ml. plasma) was as follows for groups of 5 rats:
That the decrease of biologically active EP in adjuvant disease (AD) plasma was not due to an EP inhibor was demonstrated by failure of AD plasma, 1) to compromise the biologic activity of sheep EP, or 2) to suppress the erythropoietic response of exhypoxic mice to 10 hours of hypoxia. Finally, the responsiveness of the marrow to EP was quantitated in rats in whom ensogenous EP was suppressed. Exogenous EP elicited a linear doseresponse curve which did not differ for control and AD rats. These data suggest that the disturbance of erythroid homeostasis in chronic disease results from a relative insensitivity of EP elaboration to erythropoietic stimuli.
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Lukens, J., Woodruff, C. Relationship between erythropoietin (EP) and erythropoiesis in chronic inflammation. Pediatr Res 5, 410 (1971). https://doi.org/10.1203/00006450-197108000-00162
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DOI: https://doi.org/10.1203/00006450-197108000-00162