In an earlier paper from this laboratory (4), it was pointed out that the splenectomized bile fistula dog showed cycles of bile pigment overproduction and anemia. Because of the very great amounts of bile pigments produced under these conditions we studied this reaction in considerable detail with the hope of a better understanding of body pigment metabolism. Our first paper (4) came to the conclusion that some obscure intrinsic factor related to the spleen was responsible for this reaction. The accompanying paper gives strong evidence that an extrinsic factor (Bartonella canis) is responsible. Splenectomy prepares the way for the Bartonella infection.Granting that Bartonella infection explains the blood destruction with resulting surplus bile pigment production, the mechanism of hemoglobin production under these conditions is of peculiar interest to students of anemia. These dogs must produce enormous amounts of new hemoglobin and red ceils during an active cycle on a diet which permits of but little new hemoglobin formation in simple anemic dogs. We have suggested that from the released hemoglobin the pyrrol aggregate is split off to form bile pigment while the globin fraction is turned over to form new hemoglobin. This proposal assumes that the body can readily produce a large excess of the pyrrol aggregate (four pyrr01 rings) and there is much evidence (1) to support this argument.To gain further information about blood destruction in bile fistula dogs we carried out a prolonged experiment with acetyl phenylhydrazine (Table 23) which gives similar results and supports the Bartonella observations.