Joanne H. Jepson

Hormonal Control of Erythropoiesis during Pregnancy in the Mouse

Summary. Increased plasma erythropoietic activity was observed during pregnancy in the mouse, first appearing on the 5th day. Reticulocytosis, increase of red‐cell volume, decrease of plasma iron and increase of the total iron binding capacity appeared on the 10th day. The major increase of red‐cell volume and plasma volume occurred during late pregnancy as the reticulocytes and plasma iron progressively decreased. Suppression of endogenous erythropoietin production in pregnant mice by hyperoxia did not completely abolish either plasma erythropoietic activity or the rise of the red‐cell volume observed in unexposed pregnant mice. Placental lactogen was found to have some erythropoietic activity and increased the plasma volume. Ovarian hormones were erythropoietically ineffective and, in fact, oestrogen appeared to inhibit the activity of placental lactogen.

Inhibition of the Stem-Cell Action of Erythropoietin by Estradiol.

Summary Injection of estradiol into poly-cythemic mice stimulated to produce endogenous erythropoietin inhibited the incorporation of Fe59 into their erythrocytes when it was injected during the stage of stem-cell differentiation, but not during the latter stages of erythroid cell development. In doses up to 20 times that of daily endogenous estrogen production, secretion of erythropoietin was not inhibited and utilization of erythropoietin by the bone marrow appeared to be blocked.

Erythopoiesis During Pregnancy and Lactation in the Mouse. II. Role of Erythropoietm.

Summary Suppression of erythropoietin secretion in lactating and normal female mice by 60% oxygen decreased their RCV and reticulocyte output and abolished plasma erythropoietic activity. In normal mice and in nonlactating postpartum mice, administration of prolactin resulted in an increase of RCV and of PV to values equivalent to those of 15-day postpartum lactating mice. Administration of prolactin to lactating mice and to normal female mice concurrently exposed to hyperoxia prevented the decrease of RCV and of PV which resulted from exposure to hyperoxia alone. The data indicate that in mice, the prolactin preparation used acted as an erythropoietic stimulant and caused a plasma hypervolemia which was not related to the action of erythropoietin.

The Mechanism of Action of Human Placental Lactogen on Erythropoiesis

A purified preparation of human placental lactogen (HPL) increased the incorporation of 59Fe into erythrocytes of polycythaemic mice, an effect which was abolished by its incubation with anti‐HPL but not with anti‐sheep erythropoietin (anti‐ESF).

Erythropoiesis during pregnancy and lactation. I. Effect of various hormones on erythropoiesis during lactation.

Summary RCV and plasma erythropoietic activity were significantly increased throughout lactation in the mouse as compared with normal female mice and with nonlactating postpartum mice. The RCV decreased and plasma erythropoietic activity disappeared rapidly in nonlactating mice. Prolactin stimulated erythropoiesis in postpartum nonlactating mice and polycythemic mice while adrenal steroids and thyroid hormone were ineffective.

RESPONSE OF THE POLYCYTHEMIC MOUSE AND POLYCYTHEMIC GUINEA PIG TO HUMAN ERYTHROPOIETIN.

Summary Fe59 RBC incorporation was increased in the hypertransfused guinea pig following administration of an extract of urine from a patient with chloramphenicol-induced hypoplastic anemia. This extract also had erythropoietic activity in the polycythemic mouse. Maximum Fe59 incorporation into erythrocytes of guinea pigs occurred when the Fe59 C13 was given 48 hours after administration of the erythropoietically active human urine extract.