556 ABXOliMALITIES IX METABOLIHU 



whole is iiisufifieiently supplied with oxygeu, lactic acid accumulates 

 in the tissues and appears in the urine, disappearing- when the oxy- 

 gen supply is restored. Lactic acid often appears after poisoning 

 with a large number of drugs, which Loewy has classified as drugs 

 whose action in the hody resembles that of lack of oxygen (arsenic, 

 phosphorus, hydrazine, chloroform, etc.). These poisons are all char- 

 acterized by causing" impoverishment of glycogen, fatty liver, and 

 acute degenerative changes especially in the liver cells and the endo- 

 thelium. Therefore the assumption seems justified that the poisons 

 and conditions which lead to lactic acid excretion depend ultimately 

 upon impairment of the interchange of oxygen in the cells. Wood- 

 yatt states that, so far as known, lactic acid has never been demon- 

 strated in any tissue in which deficient oxygenation can be excluded, 

 and regards lactic acid as the metabolite of asphyxia or its equivalent. 

 Over against this view is that of Embden and his associates, which 

 is shared b^- others, that lactic acid is a normal intermediary in the 

 breakdoA\Ti of the sugars in the body, its direct antecedent being a 

 triose, but perusal of their work only emphasizes that in all the con- 

 ditions in which their data were obtained asphyxial conditions were 

 present; furthermore, this conception of lactic acid as a chief inter- 

 mediate in normal sugar catabolism is not in harmony with the best 

 ideas of carbohydrate chemistrj^ (Woodyatt). This author has fur- 

 thermore found, by direct observation of the utilization of lactic acid 

 wdien injected intravenously, that it cannot well be an important inter- 

 mediate in carbohydrate catabolism. ^^"^ 



It is possible that the presence of lactic acid in the urine may also 

 result from defective transformation of ammonia into urea by a dis- 

 eased liver, the acid neutralizing, and being excreted with, the am- 

 monia; in this case no defective oxidation need be assumed. How- 

 ever, administration of phlorhizin to phosphorus poisoned dogs causes 

 both ammonia and lactic acid to disappear from the urine, indicating 

 that the ammonia is the protective substance which neutralizes the 

 lactic acid, and not the reverse. 



Sarcolactic acid, which is dextrorotary, must be distinguished from 

 its optical isomer, the inactive lactic acid that is produced by fer- 

 mentation. AVhen this fermentation lactic acid is formed in the stom- 

 ach and enters the blood, it ordinarily, like other ingested organic 

 acids, is combined by the blood alkalies and oxidized to carbonates. 

 It is doubtful if it ever enters the urine.*" 



As a general rule sarcolactic acid is not found abundant in the 

 urine together with the acetone bodies, but is, indeed, antiketogenic. 

 Its appearance in the ui-ine indicates tliat glycogen is not com]ilctoly 



■•^th TTarvey Society Lectures, lOlG. 



<" Tlie theory of Boix that cirrhosis of (lie liver may he jirodiiced by butyric 

 acid formed in fiastric ferment^Ttictn coiild im< lie corroborated bv Joaniiovics, 

 Arch. int. Pharmacodyn., 190.') (l.'j), 241. 



