166 LOUIS BAUMAN 



the general circulation and then it is excreted by the kidneys. In con- 

 ditions causing a rapid disintegration of red blood cells, as in pernicious 

 anemia, hemolytic jaundice, internal hemorrhage, etc., a large amount of 

 hematiii is converted into bilirubm, and this permits an increased ab- 

 sorption of urobilin from the intestine. Under these circumstances some 

 urobilin may escape into the general circulation even though the liver be 

 functionally intact. In recent years hematin and bilirubin have been 

 demonstrated in the blood serum in pernicious anemia (Sclmmin). 



While the enterogenous theory explains most of the known facts it 

 does not satisfactorily account for all of the experimental results recorded 

 in the literature. Fischler (a) (b) (1006, 1908) has submitted evidence 

 favoring the liver itself as a site of urobilin formation. The following ex- 

 periments may be cited in this connection : When the common bile duct of 

 dogs is tied and a biliary fistula is established it is found that in spite of 

 the deviation of the bile to the exterior urobilin persists in the stool but 

 disappears from the bile. If, to such animals, poisons that exert a par- 

 ticularly destructive effect en the liver parenchyma such as ethyl alcohol, 

 amyl alcohol and phosphorus, be administered there results a large in- 

 crease in the urobilin content of the bile and a lesser increase in the feces. 

 Fischler maintains that under these conditions the liver itself produces 

 urobilin some of which is absorbed by the blood and excreted into the 

 intestine. The disturbing features in Fischler's experiments were the 

 lack of uniform results, the licking up of bile from the fistula by some 

 of the dogs and the presence of jaundice in others. While Fischler believes 

 that the liver may form urobilin he concedes that the intestines are the 

 usual site of its synthesis. Meyer-Betz criticizes Fischler's conclusions 

 and seeks to explain all of his results by assuming that some bilirubin 

 reached the intestine by way of the blood because of the common occurrence 

 of .jaundice in bile fistula dogs. Wilbur and Addis have, in a measure, 

 substantiated the work of Fischler. They observed an increased excretion 

 of 'urobilin in the stool (and occasionally in the urine) of a dog that had 

 cirrhosis of the liver. Further, they found that when the common I "^ 

 duct was ligated the urobilin at first disappeared from the stool only to 

 retitm later in diminished quantities, and that when a biliary fistula was 

 produced in these animals the urobilin of the stool decreased but did not 

 wholly disappear. 



The arguments in favor of the so-called histogenic theory, which 

 ascribes the formation of urobilin to the tissues, appear to be weak and 

 inconclusive. The occurrence of urobilinuria after internal hemorrhage, 

 for instance, is better explained by the enterogenous theory. 



Determination. The method of Wilbur and Addis is now commonly 

 employed in this country for the determination of urobilin in the stool, 

 bile and urine. The principal steps involved are as follows (the reader 

 is referred to the original for all details) : 10 c.c. of the 24-hour volume 



