632 LEWELLYS F. BAKKEE 



production and ammonia elimination; (2) the study of the nitrogen 

 partition in the urine; (3) the search for abnormal products of protein 

 metabolism that could be responsible for the intoxication in tetany. 



The Production and Elimination of Ammonia in Tetany. That the 

 ammonia of the blood and of the urine is increased in amount in many 

 cases of tetany has been asserted by a number of investigators (Berkeley 

 and Beebe (a), Frouin, Carlson and Jacobson, MacCallum and Voegtlin, 

 Medwedew, J. B. Cooke (c), Falta and Kahn, and Morel), though other 

 observers (Albertoni, Greenwald (a)) think that too much emphasis has 

 been placed upon increased production and excretion of ammonia. Berke- 

 ley and Beebe pointed out the resemblance of the syndrome in tetany to that 

 producible by ammonia intoxication ; the symptoms of both can be amelior- 

 ated by the administration of salts of calcium or of strontium. Frouin 

 suggested that tetany may be due to intoxication with carbaminic acid. 

 Carlson showed that the livers of animals exhibiting tetany have less than 

 normal power to destroy ammonia (in experiments in which the overliving 

 liver was perfused with blood to which ammonium carbonate had been 

 added), but subsequent studies by Carlson and Jacobson indicated that 

 there is no increase in the ammonia of the blood of the dog during tetany 

 attacks and that, moreover, essential differences exist between the true 

 tetany syndrome and the syndrome resembling tetany that is produced by 

 poisoning with ammonia. 



An increase of ammonia in the blood and in the urine seems to point 

 to the catching up of ammonia out of intermediary metabolism, after the 

 deamidization of the amino acids into which protein is degraded during 

 digestion, so that the liver cannot make use of it in the formation of urea. 

 Usually such a catching up of ammonia in intermediary metabolism is due 

 to the existence of an acidosis. We have remarkable examples of this, not 

 only in the acidosis of diabetes mellitus, but also in other forms of acidosis. 

 Cooke was able to demonstrate the presence of lactic acid in the urine in 

 parathyroidectomizecl animals at the times when the ammonia excretion 

 was increased, an observation that has been confirmed by Morel, who also 

 found that the lives of such animals could be definitely shortened by aggra- 

 vating the acidosis through the administration of oxybutyric acid, or defi- 

 nitely lengthened by combating the acidosis through the administration of 

 sodium bicarbonate. On the other hand, Grant and Goldman, working in 

 Erlanger's laboratory in St. Louis, have been able to produce tetany attacks 

 through deep breathing and found that these attacks were accompanied 

 by an alkalosis. The careful metabolic studies of Isador Greenwald, of 

 New York, revealed no increase of the ammonia of the blood after para- 

 thyroidectomy. He found a slight increase of ammonia in the urine, along 

 with an increase of certain unidentified nitrogen products in the urine. 



The Nitrogen Partition in the Urine in Tetany. Studies of the nitro- 

 gen partition in the urine in the acute stage of tetany have shown that 



