586 METABOLISM, NUTRITION AND DIETETICS 



in dogs with Eck's fistula it rises to i : 8 to 1 : 33. If the animals 

 are kept on a diet poor in proteins, no symptcms may develop for 

 a considerable time. But if much protein is given, characteristic 

 symptoms, including convulsions, always appear. These may be 

 produced by the saturation of the organism with ammonia com- 

 pounds, which are formed from the proteins as in the normal animal, 

 but which the liver, with its circulation crippled, is unable to cope 

 with, and to completely change into urea, although the statement 

 has been made that when ammonia or ammonium salts are injected 

 into the blood larger quantities must be present to produce these 

 symptoms than are found in animals with the Eck's fistula. 

 Although the portal vein carries to the liver a greater supply of 

 blood than the hepatic artery (about twice as much, according to 

 Opitz and Macleod and Pearce), ligation of the latter causes a 

 greater diminution in the ratio of the amount of urea to the total 

 nitrogen in the urine than ligation of the former. While the blood 

 of the hepatic artery is, of course, nearly saturated with oxygen, 

 that of the portal vein is not half saturated, so that the total quan- 

 tity of oxygen transported to the liver by the hepatic artery is 

 actually greater than the quantity transported by the portal vein. 

 This indicates that a good supply of oxygen is an important factor 

 in the formation of urea in the liver (Doyen and Dufourt). But 

 this is no proof that the process by which it is formed is an oxidation. 

 The work of the liver, like that of other tissues, is no doubt deranged 

 by lack of oxygen. 



(6) In acute yellow atrophy, and in extensive fatty degeneration 

 of the liver, urea may almost disappear from the urine, and leucin, 

 tyrosin, and other amino-acids may appear in it along with a much 

 larger amount of ammonia than normal. Here it may be supposed 

 that the amino-acids and ammonia formed in the intestine in 

 the digestion and absorption of proteins, perhaps also amino-groups 

 formed in the tissues which would normally be culled from the blood 

 by the hepatic cells for the manufacture of urea, pass unchanged 

 through the degenerated liver, and are excreted by the kidney. 



It would, however, be very easy to overdo this argument ; for it 

 is sometimes observed that in pathological and experimental condi- 

 tions in which the liver has suffered severely considerable quantities 

 of urea continue to be excreted. Urea does not entirely cease to 

 be produced even when the liver is removed; and it must again 

 be pointed out that there is reason to believe that the formation 

 of urea is not a function peculiar to the liver, but one shared prob- 

 ably with all tissues. The liver certainly does not arrest the whole 

 of the amino-acids coming from the alimentary canal ; for the non- 

 protein nitrogen in the muscles is distinctly increased during the 

 absorption of amino-acids, and the muscular tissue, even when freed 

 from blood, contains some urea, which in all probability is formed 



