An experimental study of hemopoiesis in necturus: Effects of lead poisoning on normal and splenectomized animals

Lead poisoning causes a selective destruction of mature erythrocytes, thereby depleting the spleen and stimulating differentiation and proliferation of erythrocytes in the blood. In conjunction with splenectomy, this intravascular erythropoiesis is markedly accelerated. During the progressive anemia and subsequent regeneration of erythrocytes in simple lead poisoning the major hemopoietic loci, spleen, mesonephros, liver, and epicardium were observed. The spleen is most rapidly affected. The red cell progenitor first present in the circulation is the hemoblast, but later numerous lymphocytes enter the blood stream and are transformed into erythrocytes. Following simple splenectomy the blood shows relatively little change. A mild regenerative activity of both erythrocytes and thrombocytes ensues. In lead poisoning after splenectomy the blood picture resembles that of simple lead poisoning. The anemia is produced more rapidly and the regeneration of erythrocytes is delayed. This study emphasizes the importance of the blood stream of Necturus as a site of red cell differentiation and proliferation, and shows that the lymphocyte may be a possible progenitor of erythrocytes and thrombocytes. Under normal conditions the hemoblast suffices as a source for red cells, but under abnormal or experimental conditions, where the demand for new cells is excessive and prolonged, the lymphocyte plays a major role.