Early erythropoiesis in foetal rat bone marrow: evidence for a liver-to-bone marrow relay.

Erythropoietic activity of foetal rat femoral marrow was examined during the last four days of intra-uterine life. Insignificant at day 18, it develops slowly thereafter until birth. In the non-suckled neonate (not older than two hours), it appears notably enhanced. In order to test the potential of the foetal marrow to develop precocious or increased erythropoiesis, the activity of the erythropoietic organ predominant at this time, the liver, was altered by modifying the level of circulating corticosteroids, which govern its function. Maturation and involution of the hepatic erythron wee prevented by corticosteroid deprivation of the foetus (maternal adrenalectomy and foetal hypophysectomy). Precocious maturation and exhaustion of the hepatic erythron was induced by submitting foetuses to corticosteroids excess from day 14. Both corticosteroid deprivation and excess increase the erythropoietic activity of the femoral marrow. This activity can reach and even exceed by day 20 of intrauterine life that in neonatal marrow. Foetal hepatic erythron misfunction can therefore initiate and stimulate bone marrow erythropoiesis. The study of circulating red blood cells demonstrates that : (1) anaemia initiates medullary erythropoietic activity; (2) this anaemia is largely corrected by the bone marrow. The regulatory mechanism is presumably erythropoietin mediated.