THE CONTROL OP THE RESPIRATION 381 



mountain sickness and many of these of pathological conditions such as 

 pneumonia or CO-poisoning. The only .opssible treatment is to raise the 

 tension of oxygen in the alveolar air sufficiently to force some into solu- 

 tion in the plasma (see page 445). 



After a time acclimatization to anoxemia occurs because of adjustments 

 which bring C H back to its normal value. These depend on excretion of 

 the excess of alkali by the kidneys and the conversion of a greater pro- 

 portion of ammonia into urea (page 650). Hasselbach and Lindhard were 

 the first to show that C H of the urine becomes reduced early in anoxemia, 

 but returns to the normal after acclimatization is established, and that 

 the excretion of ammonia is also relatively decreased but remains low 

 even after acclimatization. Haldane, Kellas and Kennaway r ' 9 have con- 

 firmed these observations by showing that the titrable acid of the urine 

 (titration with No. 1 alkali to the neutral point with phenolphthalein be- 

 fore and after addition of formalin Folin's method) is reduced by one- 

 half, or more. The diminution in the NH 3 excretion found by both groups 

 of workers is always observed when the excretion of fixed alkali is in- 

 creased in proportion to the acid and it indicates that the function of the 

 liver and other organs which are responsible for conversion of NH 3 to 

 neutral urea, must become stimulated as a protection against the alkalosis. 

 The question therefore arises whether the relative decrease in the acid ex- 

 cretion by the kidneys, rendering the urine more alkaline, runs parallel 

 with the diminished production. To answer this question the ratio of 

 ammonia to acid was calculated in the experiments of Haldane, etc. (i. e., 

 the percentage of the total NH 3 and acid that is represented by NH 3 

 alone) and found to rise markedly. Therefore, the conversion of NH 3 

 into urea did not occur as promptly as the increased excretion of alkali 

 by the kidney. Part of its delay is no doubt dependent upon the time 

 required for the ammonia already present in the blood and tissue fluids 

 to be excreted before the increased urea formation could become evident 

 in the urine. The results as a whole show that the kidneys and liver on 

 the one hand, and the respiratory center on the other, respond to changes 

 in CH of the blood which are far below those that can be detected by 

 existing physical or chemical methods of measurement (Haldane). The 

 respiratory center constitutes the first line of defence against any change in 

 C H by increasing or decreasing the rate at which C0 2 is blown off from the 

 blood. The kidneys constitute a second defence by altering the ratio of 

 acid base which they allow to pass into the urine, and the liver and other 

 organs form a third line of defence by altering the amount of free NH 3 

 which they permit to enter the blood. The readjustment of the alveolar 

 C0 2 and of the acid and ammonia excretions do not return to the normal 

 until some time after the subject has been breathing at normal barometric 

 pressure. This will be made evident by consulting Fig. 142-A. 



