MARCEL NENCKI, 1847— 1901 525 



which it is brought about ? These were the questions which 

 Nencki set about solving many years after his first experi- 

 ments with Schultzen on the subject, and when in St. Peters- 

 burg he had the advantage of the co-operation of Pawlow with 

 his great surgical skill. 



Nencki had already shown that putrefactive organisms cause 

 the elimination of ammonia from the products of tryptic diges- 

 tion, but he had also demonstrated, in conjunction with Madame 

 Sieber and Macfadyen, that such organisms were not necessary 

 for the normal assimilative processes. It remained, therefore, to 

 seek for a locality where, supposing ammonia to be a precursor 

 of urea in the animal body, the elimination of this body from 

 the products of tryptic digestion could take place. Furthermore, 

 in the event of the formation of ammonia, and ammonium 

 carbonate (or carbamate), it was necessary to determine which 

 organ was responsible for the conversion into urea. At the 

 time the experiments dealing with these points were com- 

 menced, it was known from the researches of Schroder and his 

 co-workers that the liver was the principal, if not the only, 

 seat of urea formation. This fact had been determined by the 

 perfusion of blood containing various nitrogenous bodies 

 through the surviving liver and the demonstration of the 

 increase of urea after the passage through this organ. Nencki, 

 Pawlow and their assistants then endeavoured to determine 

 what would happen supposing the liver were thrown out of the 

 normal circulation. For this purpose they joined the portal 

 vein with the vena cava inferior (Eck's fistula), and showed that 

 the animal could be maintained in moderate health under these 

 conditions provided that it did not receive a heavy protein 

 diet. If, however, it was given a large meat diet, it rapidly 

 developed toxic symptoms, and showed an increased ammonia 

 output in the urine. These same toxic symptoms could be 

 produced in a normal animal by the intravenous injection of 

 ammonium carbonate, but not by the introduction of this body 

 directly into the stomach. In the dog with the Eck fistula, 

 however, the toxic symptoms were produced by the direct 

 introduction of the carbamate into the stomach. These results 

 indicated, therefore, that ammonium carbamate: is a precursor 

 of and is converted by the liver into urea ; the toxic product 

 of protein degradation is thereby converted into a harmless 

 body. 



34 



