198 RESPIRATION 



As the kidneys are essentially concerned in the regulation of the 

 reaction within the body, it is evident that failure of the kidneys 

 may cause serious disturbance of reaction. As, moreover, normal 

 human urine is acid, and presumably is so in all animals if food is 

 not taken, the disturbance will naturally be in the direction of 

 producing acidosis. Hyperpnoea and other symptoms suggestive 

 of acidosis are commonly met with as an accompaniment of serious 

 inflammation of the kidneys; and these symptoms are now com- 

 monly attributed to acidosis. One peculiarity of them is that there 

 may be little or no increase in the ratio of ammonia to total nitro- 

 gen excreted. 



Considerable new light is thrown on the causes of acidosis by 

 quite recent experiments of J. B. S. Haldane.^''^ The experiments 

 consisted in taking large doses of NH4CI during two or three 

 days, so that an abnormal percentage of ammonia was present in 

 the blood. As a result there were very pronounced respiratory 

 and other symptoms of acidosis, including a marked fall in the 

 available alkali of the blood. Owing to the excess of ammonia in 

 the blood part of the ammonia of the NH4CI had been converted 

 into urea, setting free much HCl into the blood. The normal 

 response in which the liver sets free ammonia into the blood on 

 the approach of acidosis was of course reversed, and though the 

 urine was very acid the kidneys were unable by themselves to 

 cope effectively with the HCl, so that acidosis resulted. 



A further result was that the supply of phosphate in the body 

 began to run short, so that the kidneys could not excrete so much 

 acid as usual for a corresponding acidosis. When neutralized 

 sodium phosphate was taken the excretion of acid was much 

 increased, and the acidosis passed off correspondingly more 

 rapidly. 



These experiments are of special interest, as they revealed a 

 practicable method of artificially producing marked symptoms 

 of acidosis in man. Previous attempts to do so by drinking large 

 quantities of dilute HCl or acid sodium phosphate had failed 

 owing to the efficacy of the physiological means of regulation. 

 It seems likely that in the acidosis of Bright's disease the forma- 

 tion of ammonia by the liver is checked by the accumulation of 

 ammonia in the blood owing to the inefficiency of the kidneys. 

 Hence the ratio of ammonia to toal nitrogen in the urine is not 

 increased. 



It follows from the facts brought forward in this chapter that 



"J. B. S. Haldane, Journ. of Physiol., LV, 1921. 



