[Regulation of erythropoiesis in the rat fetus: role of spleen and bone marrow in case of deficiency of hepatic erythropoietic activity].

Abstract

At the end of intra-uterine life in the rat, hepatic erythron evolution is governed by corticosteroids and it is experimentally possible to prematurely deprive the foetus of a large part of its hepatic erythropoietic tissue by inflicting repeated stress in the pregnant animal. This experimentally induced deficiency of the hepatic erythron leads to an anticipated erythroid activity in the bone marrow. Splenectomy in such fetuses has shown that the spleen does not play a major role in producing circulating anucleated erythroid cells before term.