Further evidence is presented, in addition to that of our previous papers, that the intestinal tract is, under ordinary circumstances, the sole place of origin of urobilin. So long as the biliary tract remains sterile the presence of the pigment in bile and urine is entirely dependent upon the passage of bile to the intestine.

Animals rendered urobilin-free by the collection of all the bile from the intubated, uninfected common duct, remain urobilin-free during and after extensive blood destruction caused by intravenous injections of distilled water, as also after reinjections of the animal's own blood, hemolyzed in vitro. No urobilin appears in the bile, urine, or feces of animals so intubated when blood destruction has been caused by sodium oleate, or by an agent, toluylenediamine, which damages the liver as well as the blood.

On the other hand, when bile flow into the intestine is uninterrupted, urobilinuria occurs during blood destruction caused in any of the ways mentioned and it parallels, both in severity and duration, the destructive process.

Merely increasing the amount of bilirubin within the intestines of healthy dogs by feeding urobilin-free bile, will lead to marked urobilinuria. The extravasation of blood into the tissues, resulting from the trauma of an operation for intubation of a bile duct, does not lead to urobilinuria in animals losing all of the bile after this operation, but may do so when only a small fraction of the bile is drained, while the remainder reaches the intestine as usual. The production of artificial hematomas, without operation, is not followed by urobilinuria, under the circumstances last mentioned, but merely by an increase in the bilirubin of the bile. The effect on the liver of the anesthetic employed during the intubation may be responsible for the difference in the two cases.

During the course of certain intercurrent infections affecting some of the intubated animals, notably distemper, there was a drop in the hemoglobin percentage of the circulating blood, accompanied by an increased output of bile pigment or further by urobilinuria, when the conditions were such that bile still reached the intestine. The findings pointed to increased blood destruction as a factor in the urobilinuria.

The evidence presented, taken with that of our previous papers, suffices to demonstrate, that urobilinuria, occurring during blood destruction, is primarily the result of an increased excretion of bilirubin from which, in turn, an unusually large quantity of urobilin is formed within the intestine. The liver fails to remove from the portal blood all of the latter pigment which is resorbed and consequently some of it reaches the kidneys and urine.

Our work has been carried out on animals with uninfected biliary tracts and livers, save for one case which has special mention. The influence of infection of the biliary tract on the place of formation of urobilin and the development of urobilinuria will be discussed in a succeeding communication.

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