Summary
The erythropoietin content in cord blood was determined from normal full term infants, fants, from infants born more than 2 weeks after term, from infants of preeclamptic, diabetic and Rh‐immunized mothers. The group of normal infants showed higher ergthropoietin levels than the premature group. Highly elevated erythropoietin levels were found in some infants in the preeclamptic, the postmature group and in the infants of diabetic mothers. The greatest frequency of increased erythropoietin levels were found in the preeclamptic group. The infants with the greatest rise in erythropoietin content often showed clinical signs of dysmaturity. Erythroblastotic infants seemed to show a rise in erythropoietin levels when capillary hemoglobin fell below 13‐11 g. The results indicate that both anemic and hypoxic hypoxia may give an increase in erythro‐poietin content, and that erythropoietin is a stimulating factor for red cell production in fetal life, at least in the last months.
Measurements were made to characterize the relationship between erythropoietin output and erythropoiesis in two groups of subjects, one moved from a sea level habitat to high altitude, and the second moved from a high altitude habitat to sea level. In the first group, there was a latent period of 6 hours followed by a rapid increase in erythropoietin, and a secondary fall to a level of approximately twice normal. The increased erythropoietin stimulus was also reflected in a shortened marrow radioiron transit time. In the second group, there was an initial unexplained rise, after which erythropoietin fell within 8 hours to undetectable amounts.
Elevated erythropoietin was associated in Group I with an increased iron uptake within 24 hours of the stimulus, suggesting a direct action of erythropoietin on hemoglobin synthesis by the existing marrow population. Limitation in erythropoiesis to a rate of less than twice normal was tentatively explained by a restricted iron supply. In the second group, marrow activity continued for 3 days despite a marked fall in erythropoietin, indicating that cells in the maturation phase completed their normal development.
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