352 THE RESPIRATION 



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

 direct excitation of the center from 2 deficiency is possible. 



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

 ter and his pupils, 23 but their objed was not so much to show the close 

 parallelism between the < '< > L . content of the respired air and the pulmonic 

 ventilation as to demonstrate the changes produced in the sensitivity of 

 the respiratory center in pneumonia. 



Possibility that CO L . Specifically Stimulates Center. — After showing 

 that CO, ads as an excitant of the respiratory center, the question arises 

 whether we are justified in the assumption thai lias been made tentatively 

 that the action depends on the raising of the C H of the blood, or whether 

 it may be a specific action of the HC0 3 anion itself. Many attempts have 

 been made to decide this question experimentally, the general principle 

 of the experiments being to determine whether C H of the blood runs 

 parallel with the CO, content of the respired air and with the hyperpnea. 

 Using the gas-chain method (page 31), Hasselbalch and Lundsgaard 22 

 found that the hyperpnea produced in rabbits by breathing in CO,-rich 

 air runs approximately parallel with the increase in the C H of the blood, 

 but on account of the experimental difficulties encountered they could not 

 decide whether changes in C H are alone responsible for the effect. These 

 authors had previously demonstrated that changes in C H can be induced 

 in blood removed from the body by alterations in the CO, tension within 

 the physiological limits. An increase of one millimeter in C0 2 tension 

 was found to cause an increase in C H of 0.0065 x 10 7 (see page 27). 



R. W. Scott's experiments, above referred to, have, however, yielded 

 more definite results. By using the colorimetric method for determining 

 Ch of the blood (see page 32), it could be readily shown, as is evident 

 from the table (col. 8 in table), that a marked rise in C H became evident 

 when the inspired air contained 5 per cent or more of C0 2 . That this 

 rise was due to increase in the C0 2 tension was shown not only by finding 

 a greater percentage of CO, (col. 15) in the blood, but also by being able 

 to demonstrate that when CO,-free air was bubbled through the blood 

 removed during the dyspnea, C H immediately returned to the normal. 

 which it also did when the blood removed after the animal had breathed 

 for a few minutes in outside air (col. 16). The CO, content likewise re- 

 turned (col. 17). Had the increase in acidity been caused by nonvolatile 

 acids — lactic, for example — these results, particularly the latter, could 

 not have been obtained. 



Although there is therefore no doubt that the C H of the blood may 

 be raised because of an increase in CO, in solution in the blood plasma — 

 a C0 2 acidosis, as we may call it (see page 354)— this does not prove that 

 the stimulation of the respiratory center is brought about solely by C H . 



