1086 EXCRETION 



(CON 2 H 4 .HN0 3 ), and on treatment with oxalic acid its oxalate (CON 2 

 H4.H 2 C 2 04+H 2 O). Urea melts at 130 C., undergoing finally a decom- 

 position which yields ammonia, biuret and cyanic acid, the latter 

 being polymerized to cyanuric acid. On hydrolysis by means of 

 heating with strong acids or alkalies, it yields carbon dioxid and 

 ammonia. 



Ammonia. The urine of man and the carnivora contains a small 

 quantity of ammonium salts which serve as a means of transfer for 

 the acid radicles which have been ingested or have been formed in 

 the body. The chief source of these salts is the ammonia of the blood, 

 derived from the nitrogenous portion of the diamidized amino-acids. 

 This ammonia is carried to the liver where urea is synthetized, but 

 some of it escapes and reaches the kidneys where it slips through into 

 the urine. Some of it is also derived from the ammonium salts in- 

 gested from the ammonia produced in the course of the intestinal 

 putrefaction of the proteins. In the body, it exists as ammonium 

 carbonate which is the precursor of urea. It is for this reason that so 

 little of it circulates, but when mineral acids are administered, or when 

 excessive quantities of acids are produced, as in diabetes mellitus, the 

 body makes use of the ammonia as a base and an extra amount of it 

 appears in the urine. An excess of alkali, on the other hand, causes 

 it to be transferred into urea and to disappear as such from the urine. 

 This accounts for the fact that it is not present in the urine of vege- 

 tarians nor in that of the herbivora. Ordinarily, the daily output of 

 ammonia-nitrogen varies between 0.3 and 1.2 grm., the average being 

 0.7 grm., or 3.5 per cent, of the total amount of nitrogen. 



Acidosis. It has been known for some years that the urine of 

 diabetics is loaded with acetone, diacetic acid and /3-oxybutyric acid. 

 It was supposed at first that these bodies are derived from glucose, 

 because they are present in glycosuria, but it is now known that they 

 are the result of a disordered process of breaking down the fats. 

 Ordinarily, this foodstuff is converted into carbon dioxid and water, 

 but in certain abnormal conditions there is produced /3-oxybutyric 

 acid, then diacetic acid and lastly, acetone. Since a small amount of 

 acetone is normally present in urine and especially after the ingestion 

 of butter consisting of the lower fatty acids, and since none of these 

 substances is poisonous, except in enormous doses, it may be asked 

 why they cause such serious disturbances when formed in the course of 

 metabolism. Briefly, the answer is this: Fats are converted into these 

 abnormal acids instead of into carbon dioxid and water whenever 

 the tissues are unable to obtain sugar from the blood. The blood is 

 normally alkaline and the functions of the tissues are adapted to this 

 particualr reaction. In consequence of the production of diacetic and 

 especially of /3-oxybutyric acid, its alkalinity is greatly reduced. The 

 functional disturbances then ensuing constitute the condition of 

 acidosis. It would seem, therefore, that an artificial supply of alkalies 

 should place the body in a position to withstand the presence of these 



