842 HAKOLD BAILEY 



Pearce and Jackson point out that the same criticism may be applied 

 to the results of Ewing and Wolf, for their cases were presumably also 

 unable to eat, and Underhill and Rand do not accept the defective deamina- 

 tion theory and attempt, to explain the abnormal ammonia figures as the 

 result of an acidosis. They detailed the report of observations on a per- 

 nicious vomiting case which was fed large amounts of glucose by rectum. 

 While marked variations occurred in the ammonia figures following the 

 administration of the sugar, nevertheless it did not control the condition 

 nor lead to a permanent lowering of this fraction and finally the uterus 

 had to be emptied. 



The Urine in Experimental Liver Necrosis 



About this time there were several experimental studies carried on 

 in an attempt to ascertain the changes in the nitrogenous metabolism 

 under various conditions of liver degeneration. Pearce and Jackson were 

 able to produce in dogs, liver degeneration of varying degree by the injec- 

 tion of toxic sera. A diffuse degeneration without necrosis was produced 

 by the injection of weak sera and resulted in a transient rise of the total 

 nitrogen of the urine with a slight rise in the ammonia fraction. With 

 the injection of older sera there was not only diffuse degeneration of the 

 cells but also areas of focal necrosis and there were very considerable 

 changes in the nitrogen excretion. The total nitrogen and the urea were 

 increased and there was a marked rise in the undetermined nitrogen. The 

 ammonia was variable but rose above the normal. They believe that 

 the liver possesses a "factor of safety" evidenced by an increase of the 

 functional activity of the unharmed cells. 



Hydrazin produces a fatty degeneration of the liver cells without 

 marked changes in other organs. It attacks first the cells about the center 

 of the lobule and it destroys a large amount of liver tissue. However, 

 a considerable portion of the tissue remains in a fair state of preservation. 

 Underhill and Kleiner gave this substance to dogs and concluded that 

 in this type of poisoning the partition of the urinary nitrogen was only 

 slightly different from that which occurs in inanition. There was a 

 marked rise in the total nitrogen and the various fractions with the ex- 

 ception of ammonia which remained about the same. The urea per- 

 centage was lower and there was an accompanying rise in the undeter- 

 mined nitrogen. In both the fasting and the hydrazin poisoned dogs 

 there was present considerable allantoin nitrogen. 



Wolf and Osterberg in an investigation undertaken to throw light 

 upon the behavior of creatin in starvation, poisoned fasting animals with 

 phlorizin. This poison produces fatty infiltration and degeneration of 

 the albumin of the liver cells. Waldvogel believes the process is closely 



