PATHOLOGICAL METABOLISM IN PKEGNANCY 837 



pation in some cases -led to a marked increase of the ammonia with a 

 corresponding decrease in the uric acid. In others the ammonia was but. 

 slightly increased. However, upon feeding amino-acids there was always 

 a decided increase in the 'ammonia, even to 70 per cent of the total nitro- 

 gen. A large amount of lactic acid was also present in the urine. From 

 these experiments it, became apparent that in geese a liver function is the 

 synthesis of ammonia to uric acid. In the absence of this organ the 

 amino-acids could be broken down to ammonia, but further changes oc- 

 curred only to a slight extent, as this particular liver function was taken 

 up by other parts of the organism. 



Hahn, Massen, Nencki and Pawlow were able to sidetrack the liver 

 in dogs by producing an Eck fistula, whereby the inferior vena cava is 

 connected with the portal vein. The animals showed marked toxic symp- 

 toms which resembled those of uremia. Some of the dogs survived and 

 on being fed meat, again had all the symptoms of intoxication which was 

 so severe that in many instances it proved fatal. The urinary nitrogen in 

 these cases was low in urea and the ammonia was increased to 10-20 per 

 cent. There was also an increased production of lactic acid and ammo- 

 nium carbamate was present in the blood although there was no reduction 

 of the carbon dioxid. On autopsy the livers were found to have marked 

 fatty degeneration and atrophy. The authors concluded that under the 

 conditions of these experiments, there was a defect in the formation of 

 urea from ammonia and an intoxication by ammonium carbamate or by 

 other precursors of urea ; and that there was indication that urea formation 

 goes on to some extent in tissues and organs other than the liver. 



This work was the beginning of many studies of the nitrogenous 

 metabolism in diseases of the liver and in 1895 the entire field was thor- 

 oughly reviewed by Minkowski(c). He collected the reports of the am- 

 monia excretion in a number of cases of liver degeneration and found that 

 the percentage increase was not great in many instances. Engelein in 2 

 cases of phosphorus poisoning found 10.6 per cent and 11.2 per cent am- 

 monia in the urine. Von Noorden(c) in 2 cases of liver degeneration 

 found 14.2 per cent and 18.1 per cent ammonia with 75.4 per cent and 71.0 

 per cent urea nitrogen. Munzer with 3 cases was able to show only 6.9 

 per cent ammonia with 91.8 per cent urea in one case, but the second had 

 17.3 per cent ammonia with 52.4 per cent urea and the third with alkaline 

 urine had 36.7 per cent ammonia with 52.9 per cent urea. Eichter(6) in 

 n. case of acute yellow atrophy found a 10 and 16 per cent ammonia excre- 

 tion with 61 per cent and 72 per cent urea. These figures are important 

 for they serve for comparison with more recent work that will be mentioned 

 later. 



Bouchard (6) in 1887 suggested that eclampsia was an autointoxication 

 due to the failure of proper excretion by the kidneys of the nitrogenous 

 products and hence their retention in the blood. Massen varied this 



