The Erythropoietin/Hematocrit Relationship in Normal and Polycythemic Man: Implications of Marrow Regulation
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While it has been suggested that orally transmitted erythropoietin can stimulate erythropoiesis, in vitro studies have shown that this glycoprotein is inactivated by incubation with various proteolytic enzymes. This study, utilizing the incorporation of 59 Fe in the plethoric mouse, suggests that orally administered erythropoietin is ineffective in stimulating erythropoiesis.
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In has been long recognized that erythropoiesis in adults is under control of erythropoietin, a glycoprotein produced mainly by adult kidneys in inverse relation to oxygen availability. Increasing evidence indicates nowadays that EPO is also an essential growth factor for red cell precursors at different sites of fetal erythropoiesis. The primary site of EPO production during fetal and neonatal life is the liver, and the fetus has been shown to be able to increase EPO production in response to hypoxia through intrinsic oxygen sensing mechanisms of hepatocytes. Thus despite different sites of both erythropoiesis and EPO production a similar oxygen dependent feedback control of red cell formation appears to operate during all stages of development. EPO levels in fetal blood are potentially useful parameters of fetal stress, and, as in adults, the availability of recombinant EPO raises the possibility to modulate erythropoiesis in the perinatal period.
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ABSTRACT. The regulation of erythropoiesis during the first three months of life was studied in 30 premature infants who had haemoglobin concentrations which were lower than in term infants of the same postdelivery age. Erythropoietin and erythropoiesis inhibitors were measured by means of an exhypoxic polycythaemic mouse bioassay. The percentage of haemoglobin F was determined as well. An increased erythropoietin level was detected only in six infants older than six weeks, whose blood haemoglobin concentration was lower than 100 g/l, while in serum from other babies erythropoietin was undetectable by the method used. Erythropoiesis inhibitors were present in 80% of the samples tested. The results presented indicate that in premature infants erythropoiesis is regulated through erythropoietin and that inhibitors of erythropoiesis take part in this regulation as well, but that the haemoglobin level at which erythropoietin is increased is lower in preterm infants than in term babies.
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While it has been suggested that orally transmitted erythropoietin can stimulate erythropoiesis, in vitro studies have shown that this glycoprotein is inactivated by incubation with various proteolytic enzymes. This study, utilizing the incorporation of 59Fe in the plethoric mouse, suggests that orally administered erythropoietin is ineffective in stimulating erythropoiesis.
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We found primary erythrocytosis in two male siblings with hematologically normal parents. To clarify the abnormalities in erythropoiesis, we studied erythropoietin production in the older sibling as well as in vivo and in vitro responses of bone marrow to various stimuli. His erythropoietin excretion after a 1000-ml phlebotomy increased by 0 to 11 units per day. In liquid-suspension culture, erythropoiesis was prominently augmented by erythropoietin and unstimulated erythropoiesis was greater and more prolonged than normal. Numbers of erythroid colonies rose in methylcellulose culture without exogenous erythropoietin, and cloning increased with added erythropoietin. Anti-erythropoietin antibody substantially decreased erythropoiesis in vitro. Increased bone-marrow erythropoiesis was also demonstrated in murine diffusion chambers. The principal abnormality in this familial erythrocytosis appears to be a greatly expanded erythropoietic precursor pool that is responsive to erythropoietin in vitro and in vivo. This abnormality is analogous to the functional erythropoietic defect in typical polycythemia vera.
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Abstract Erythropoiesis was obtained in murine long‐term bone‐marrow cell cultures (LTBMCs) in the presence of erythropoietin (Epo) when the medium was frequently renewed. The level of the erythropoietic differentiation was shown to be a function of the erythropoietin concentration. In response to Epo addition, an activity which stimulates CFU‐E proliferation in semisolid cultures of fresh bone marrow cells was detected in the LTBMC supernatants. These results suggest that another factor, whose synthesis may be under Epo control, participates in the stimulation of erythropoiesis in vitro.
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The injection of testosterone into polycythemic mice produces a small but significant stimulation of erythropoiesis, as measured by Fe59 uptake into the peripheral blood, if the interval between the injection of the hormone and Fe59 is 96 hours. This stimulation of erythropoiesis is completely abolished by the injection of immune serum against the hormone erythropoietin.
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