THE CONTROL OF THE RESPIRATION 367 



There is an obvious reason why the adjustment of pulmonic ventilation 

 should not depend primarily upon changes in 2 supply to the respira- 

 tory center. If it were so, many other tissue activities and other nerve cen- 

 ters would suffer from the 2 deficiency before there was time for the 

 breathing to become stimulated sufficiently to make good the loss of 2 . As a 

 matter of fact, headache, dizziness, nausea and even fainting are almost 

 certain to be caused whenever any muscular exercise is attempted in an 

 atmosphere containing a deficiency of 2 but no excess of C0 2 (cf. moun- 

 tain sickness). An adequate 2 supply of the body is, therefore, insured 

 by changes in C0 2 tension of the blood. 



Quantitative Relationship between C0 2 of Inspired Air and Pulmonary 

 Ventilation. These results suggest, as the next step in the investigation 

 of our problem, the determination of the quantitative relationship be- 

 tween the C0 2 percentage of the respired air and the amount of air 

 breathed (pulmonic ventilation).* That there is such a relationship has 

 been most successfully demonstrated by R. W. Scott, 20 who used for his 

 purpose decerebrate cats.f The trachea was connected, through a T-tube 

 provided with valves, with tubing leading to a large bottle and a Gad-Krogh 

 spirometer, so that the animal breathed out of the bottle into the 

 spirometer, these two being also connected together. The spirom- 

 eter was made to record its movements on a drum, so that an accurate 

 record of the depth and frequency of the respirations was secured. Sam- 

 ples of air were removed from the bottle by ground-glass plunger syringes 

 at frequent intervals during the time that the animal was respiring into 

 the tubing. 



The results are given in the accompanying curve (Fig. 129), which shows 

 that there is a perfect correspondence between the C0 2 percentage in the 

 air of the bottle and the pulmonary ventilation. Moreover, when the 

 bottle was filled with 2 instead of air to start with, the same results 

 were obtained, showing that the C0 2 accumulation alone was responsible 

 for the hyperpnea. In these cases the percentage of 2 remaining in the 

 system after hyperpnea had become extreme, was far above that at which 

 excitation of the center as a result of 2 deficiency is possible. 



Experiments of a similar type had previously been performed by Por- 

 ter and his pupils, 21 but their object was not so much to show the close 

 parallelism between the C0 2 content of the respired air and the pulmonic 



*A distinction is somewhere drawn between pulmonic ventilation and alveolar ventilation, the 

 former being the total amount of air that enters and leaves the lungs, and the latter, that which en- 

 ters and leaves the alveoli. This distinction is based on the assumption that the capacity of the dead 

 space may vary considerably from time to time, which, as pointed out elsewhere, is erroneous. For 

 practical purposes pulmonic ventilation is the safer value to give. 



fDecerebrate animals must be used in these experiments, since anesthetics markedly depress the 

 activity of the respiratory center. 



