i'.oS THE RESPIRATION 



2 the excitability of the center is raised (i.e., its "threshold" lowered), 

 so that LI becomes stimulated by Ch, to which ordinarily it does not re- 

 spond. We shall now proceed to examine the experimental evidence 

 bearing on these possibilities. 



V>y examination of the alveolar air of an individual confined in a pneu- 

 matic cabinet in which the barometric pressure is gradually lowered, 

 it has been found that although the C0 2 tension remains constant for 

 a considerable range (cf. page 356), it begins to fall when the barometric 

 pressure has reached about 550 mm. Hg. At this pressure the tension 

 of Oo in the alveolar air will be 62 mm. instead of its normal of about 

 105 at atmospheric pressure. Below it the alveolar C0 2 tension quickly 

 falls, and at the same time hyperpnea becomes evident, although the 

 person himself may be unaware that he is breathing more deeply. If 

 this experiment is repeated with the difference that, as the pressure is 

 lowered, an excess of 2 is introduced into the chamber, the hyperpnea 

 dues not supervene until a barometric pressure has been reached that is 

 distinctly lower than when no excess of 2 is present, and at the same 

 time the C0 2 tension in the alveolar air remains unchanged. The ex- 

 planation of this result is that by lowering the 2 tension in the alveolar 

 air and. therefore, in the blood and tissues, oxidative processes become 

 depressed so that unoxidized acids, such as lactic, accumulate in the 

 blood and by adding their effect to that of the C0 2 serve to raise the C H 

 of the blood. As a result, the respiratory center becomes excited, hy- 

 perpnea supervenes, and the volatile CO, is removed from the blood into 

 the alveolar air. On supplying 2 artificially, this failure of proper 

 oxidation does not set in and breathing goes on normally. 



In the above experiment there must be a period during which the 

 I '< >._. tension of the alveolar air tends to become increased — namely, when 

 the fixed acids first appear and decompose the carbonates of the blood. 

 This increase is prevented by the more thorough alveolar ventilation. 

 When a person is kept in such a chamber for some time at a pressure 

 which causes a diminution in the alveolar C0 2 tension, the tension does 

 not immediately return to its oormal Level when atmospheric air is again 

 breathed, indicating thai the fixed acids are only slowly got rid of. 



The second hypothesis — namely, that the 2 deficiency directly raises 

 the excitability of the respiratory center — has many advocates, among 

 them Lindhard, 25 who found that, when the percentage of 2 in the alve- 

 olar air Avas raised, a higher percentage of C0 2 was necessary to cause 

 an increase in the ventilation of the lungs, and conversely, that a distinct 

 increase in the excitability of the center occurred when the inspired air 

 contained less than the normal percentage of ( ) L .. Although it is ad- 

 mitted by Haldane and his school that such alteration in the excitability 



