THE FUNCTIONS OF THE LIVER AND SPLEEN 449 



Immediately brought on signs of surliness, and eventually induced 

 convulsions. 



(4) In certain forms of liver disease the amount of urea passed in 

 the urine is markedly diminished, the amount of ammonia bodies 

 being correspondingly increased. 



(5) Perfusion of blood-containing ammonium carbonate through 

 the liver of a mammal leads to a marked increase in the urea content 

 of the blood. This experiment was done originally upon the liver of 

 a dog, but it holds true for all mammals. According to some autho- 

 rities, ammo-acids, such as glycin, alanin, arginin, also lead to the 

 formation of urea when perfused through the isolated liver. This, 

 however, is not accepted by all at any rate, as a normal process. 



Urea, therefore, is undoubtedly formed in the liver, the main 

 precursor being compounds of ammonia. These compounds are 

 particularly the carbonate, which may be graphically represented as 



m ONH 4 

 X ONH 4 



and the carbamate, which may be figured as 



m /ONH 4 

 \NH 2 



The change to urea may probably, therefore, be represented as 

 follows : 



ONH 4 _ ONH 4 _ rn 



\ONH 4 NH 2 NH 2 



Ammonium carbonate Ammonium carbamate Urei 



Some of the urea formed in the liver may be derived from the 

 conversion of uric acid to urea. It has been shown in the laboratory 

 that creatin may give rise to urea. There is, however, no good 

 evidence to show that such is the caee inside the body. 



Most of the urea formed in the liver is derived from the nitrogenous 

 part of the food taken in that is to say, it is exogenous in origin. 

 Alterations in the amount of nitrogenous food cause similar fluctua- 

 tions in the amount of urea in the urine (see p. 455). The view held 

 AS to the form in which the precursor of urea reaches the liver 

 depends naturally upon which hypothesis of protein metabolism 

 is put forward. According to the first view (p. 424), urea would 

 be derived mainly from the amino-acids brought to the liver by 

 the portal blood, particularly from such amino-acids as gtycin, 

 alanin, leucin, and arginin. According to the other view, no such 

 acids exist in the portal blood. The precursor of most of the urea 

 formed in the liver would in this case be the ammonia which has 

 been broken off from the excess amino-acids during the prooess of 

 their deaminization in the intestinal mucous membrane. This is 

 transported to the liver in the form of the carbonate and carbamate, 

 and converted into urea. Some urea might also be formed from 

 excess amino-acids left over in r the bloodstream after a tissue has 



29 ' 



