620 METABOLISM 



are being absorbed or produced. As we shall see later, this criticism is 

 particularly applicable in the case of sugar. Even during the injection 

 of considerable quantities of sugar into the portal vein, no difference 

 in percentage can be demonstrated between the blood of the two sides 

 of the liver, although we know that sugar is being retained to form 

 glycogen. For the same reasons, differences in the percentage amounts 

 of amino acids or of urea are often difficult to demonstrate in the blood 

 entering and leaving the liver even when we know that large quantities 

 of them are being added to or removed from it. 



Clinical. Since the liver is an important seat of urea formation, the 

 question arises as to whether the relative percentage of urea and am- 

 monia in the urine will become altered by disease of the liver. Many 

 observations with this point in view have been undertaken, but it can 

 not be said that the results are very striking. In extreme destruction, 

 such as that produced by phosphorus poisoning, there may indeed be 

 a great increase in the relative amount of ammonia and a decrease in 

 that of urea. The same is true in acute yellow atrophy of the liver, in 

 which disease the nitrogen excreted as ammonia may amount to as much 

 as 70 per cent of that excreted as urea. In milder forms of liver dis- 

 turbance, however, such as cirrhosis, the figures are much less striking. 

 When an increased ammonia excretion is observed in such cases, we 

 must be cautious in drawing the conclusion that it is due primarily to 

 abolition of the hepatic function. It may just as well be caused by the 

 development of acids in the organism that require the ammonia for 

 their neutralization. It is significant, for example, that considerable 

 quantities of acids are produced in phosphorus poisoning. 



Although the urea and ammonia excretions become altered by exten- 

 sive destruction of liver tissue, it is a remarkable fact that very little if 

 any change occurs in the amino nitrogen, either of the urine or of the 

 blood. In experimental necrosis of the liver produced by chloroform 

 or by phosphorus, it is only in the latest stages of the condition and 

 when it is of the very severest type that an amino-acid increase has been 

 found to occur in the blood and urine. The conditions seem to be some- 

 what different in man, abnormally high amounts of amino nitrogen hav- 

 ing been observed in the blood in a considerable proportion of patients 

 with impaired liver function. In very severe cases of diabetes, for ex- 

 ample, figures that are distinctly higher than normal have been observed 

 (Van Slyke, etc.). In eclampsia the marked pathological changes in the 

 liver might be expected to be associated with an upset in the metabo- 

 lism of amino acids. Losee and Van Slyke 35 have, however, recently 

 shown by the most accurate methods that neither in the blood nor in the 

 urine is any excess of amino acids to be found in this condition, although 



