We studied changes in the erythroid hemopoietic stem during phenylhydrazine-induced hemolytic anemia. Stimulation of erythropoiesis was associated with increased functional activity of erythroid precursors, which resulted from changes in feeder capacity of hemopoiesis-inducing microenvironmental cells and erythropoietic activity of the plasma. The development of encephalopathy induced by a hemolytic poison was accompanied by a decrease in hyperplasia of bone marrow erythropoiesis. It was related to a decrease in the number of proliferating erythroid precursor cells. These changes accompanied the increase in the secretory function of adherent myelokaryocytes, rise in erythropoietic activity of the plasma, enhanced formation of erythroid hemopoietic islets, and accelerated maturation of hemopoietic cells.