Experimental infection of the intubated and previously sterile biliary tract of the dog with particles of the stools leads to a formation of urobilin from the bilirubin of the bile as it flows through the ducts. No urobilinuria occurs, however, unless temporary biliary obstruction is produced, or the liver parenchyma injured. Then urobilinuria develops, despite the fact that no bile is reaching the intestine and, by corollary, no urobilin being formed there.
Cholangitic urobilinuria, as one may term the phenomenon just described, to distinguish it from the urobilinuria having origin in pigment absorbed from within the intestine, is far more pronounced in animals possessing a healthy gall bladder than in those with a pathological gall bladder or with one prevented from functioning by severance of the cystic duct. These facts suggest that there may be an active absorption of urobilin from the normal gall bladder. There can be no doubt that the pigment is absorbed from within the bile ducts.
There is no evidence whatever to justify the belief that urobilin is ever formed through the action of liver parenchyma. There may conceivably be an intralobular formation of the pigment consequent upon the activity of bacteria within the liver tissue, though such a happening has yet to be demonstrated.
Utilizing the gall bladder as a conduit in treating biliary obstruction: a historical perspective