The pattern of stem cell repopulation in heavily irradiated mice receiving transplants of fetal liver.

E RYTHROPOIESIS IN THE NEWBORN RAT is in many respects analogous to that seen during the fifth-sixth month of gestation in human beings. Thus, up until birth, the red cell production in the rodent is predominantly hepatic and only at birth does significant myeloid erythropoiesis commence. This appeared to offer the opportunity to evaluate regulation of fetal red cell production. Initially we observed that bilateral nephrectomy in the neonatal rat does not produce the erythroid aplasia characteristic of the renoprival adult rat.1 This, in part, might be explained by extrarenal erythropoietin production which has been recently demonstrated in the newborn rat.2 The failure of plethora and starvation3 to produce in the newborn animal the degree of erythroid aplasia seen in the adult might be accounted for by the failure to significantly alter the 02 supply-demand relationship due to the high metabolic rate seen in the growing animal. In an effort to circumvent these problems we turned to transplantation of fetal tissues in a heavily irradiated adult animal. We have observed a difference in the recovery pattern of erythropoiesis in the recipients of fetal liver as compared with those of adult bone marrow.4 In part, these differences might be attributed to a difference in the generation time. Accordingly, we have compared the growth curve of hematopoietic stem cells derived from fetal liver with that of adult bone marrow.