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In dogs intubated for the collection of all of the bile, a marked falling off in the yield of bilirubin is regularly to be noted after operation, followed soon by an anemia of secondary character. Though, in the absence of complications, the anemia is mild, it persists despite the excellent general condition of the animal. Intercurrent changes in the hemoglobin percentage take place from time to time, and these are accompanied by very similar fluctuations in the bilirubin quantity. At first inspection the data strongly suggest that blood destruction finds accurate quantitative expression in the yield of bile pigment. But this is not the case. True, the destruction finds expression in terms of bile pigment and practically at once; and the data support the conception that bilirubin has no other sources besides the hemoglobin of destroyed blood. But our experiments show that the amount of it put forth during the development of an anemia from gradual blood destruction, either intercurrent or induced, is far below that derivable from the net quantity of hemoglobin disappearing from the circulation. The discrepancy is referable to a process of pigment conservation which varies in proportion to the body need. We have shown in a previous paper that bile pigment may on occasion beabsorbed from the intestinal tract. This fact and those reported in the present communication lead one to question the accepted view that bilirubin is mere waste material eliminated by way of the liver. The anemia which develops upon total loss of the bile is not improbably consequent on the pigment loss therewith. Current methods of computing the rate of normal and pathological blood destruction from the bilirubin (or urobilin) yield are unsound in principle and open to large error in practise. Yet there is no doubt that day-to-day variations in the output of bile pigment result from changes in the blood; and on occasion they provide enlightening evidence of the nature of hemic events.
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