ENDOGENOUS UROBILIN METABOLISM 557 



over a period of four days, produced much too small an excretion of urobilin 

 on the days it was given, and none afterward, while in a second instance the 

 increase of urobilin excretion in the period following its administration was 

 much too large. 



Nevertheless, the consistent finding of abnormally high urobilin 

 excretion in a particular disease establishes increased hemoglobin 

 breakdown beyond doubt; the method has been used by many workers 

 and all agree that it supplies a rough measure of hemoglobin break- 

 down {1007, 2969, 2987, 2988:2989, p. 2509). The increase of urobilin 

 excretion in relap.se in pernicious anemia (038,7^0,2969) must be 

 considered as evidence for increased hemoglobin destruction in this 

 disease; the same holds for aplastic anemia (2235). The destruction 

 of erythrocytes need not necessarily occur in the circulating blood 

 — it may involve young hemoglobin-containing bone marrow cells 

 before their escape into the circulation - — but destruction there is. 

 The results cannot be explained, as has been tried by Patek and 

 Minot (2118), by Isaacs (1384), ^iid by others, by assuming that 

 urobilin is formed from an unused precursor of blood pigment syn- 

 thesis (cf. Section 6..S.). 



Conversely, increase of red cell destruction is unlikely if no abnor- 

 mally high urobilin excretion is found, e.g., in anemia of sepsis (2862). 

 After hemorrhage the urobilin excretion is diminished (503). 



9. 2. .5. Urol)iIin in Blood Plasma. So far we have discussed the fate of 

 urobilin which is reabsorbed by the liver and finally excreted in the 

 intestine; it remains to discuss the fraction which enters the general cir- 

 culation and which is finally excreted in the urine. Normally this fraction 

 is much smaller, at least as far as can be judged from the urinary excretion; 

 in liver diseases, however, .30% or more of the urobilin may appear in the 

 urine. 



The concentration of urobilin in normal blood is so small that it cannot be 

 demonstrated by the fluorescence of its zinc salt [12 20. 237 8, 3 100), although 

 the contrary has repeatedly been claimed. If the liver is traumatized in 

 liver diseases, and in severe infections and in moribund patients, urobilinemia 

 develops {3100: cf. 2US'.). p. '-2.>>3). 



By spectrophotometry Heilmeyer and Olilig (1220) established the pres- 

 ence of urobilin in the plasma in liver disease, but the concentration never 

 reaches high values (maximal 0.4li milligram per cent). Heilmeyer (1213, 

 p. 198) and Farmer-Loeb (7.i.'>) found urobilinogen in the plasma of patients 

 with severe urobilinuria. Watson (2!)S3) observed that the Ehrlich aldehyde 

 reaction of the plasma became positive '■2()-3() minutes after the intravenous 

 injection of /-tetraliydromesobilcne, while the urobilin band disappeared. 

 Probably, tlierefore. urobilinogen, not urol)ilin, is present in the blood. 



Urobilin injected intravenously disappears rapidly from the blood (23o0, 



