374 THE RESPIRATION 



merely show a steadily increasing hyperpnea is probably due to the un- 

 equal rates at which the 2 and C0 2 tensions change in the blood. Be- 

 cause of a "buffer action" the latter fluctuates much less than the for- 

 mer. Another cause for the periodicity is no doubt the delay between 

 the gas exchange in the lungs and the arrival of the blood in the brain. 

 When the 2 tension of the blood supplying the respiratory center falls 

 to so low a level that excitation of the center occurs, the resulting in- 

 creased breathing aspirates outside 2 into the alveoli. After a moment 

 or so, the 2 is carried by the blood to the 'center, so that its stimula- 

 tion by 2 deficiency is removed, and it is left in a condition in which 

 it fails to discharge any impulses, since there is a subnormal C H of the 

 blood as a consequence of the lowering of the C0 2 tension produced by 

 the hyperpnea. A little time must now elapse before the C0 2 again 

 rises or the 2 falls sufficiently to excite the center. 



Fig. 133. Quantitative record of breathing air through a tube 260 cm. long and 2 cm. in diameter. 



(From Douglas and Haldane.) 



A similar although less marked degree of periodic breathing can 

 sometimes be obtained by merely respiring through a long tube without 

 any provision for the absorption of C0 2 . In this case it is more difficult 

 to explain the cause of the periodic breathing, but that the main factor 

 concerned is one of 2 deprivation is evidenced by the fact that in this 

 as in the previous experiment, the periodic nature of the respiration is 

 immediately changed to the regular breathing if 2 is introduced into 

 the tube. The interest of the experiment lies in the fact that a similar 

 relative elongation of the dead space is probably accountable for the 

 periodic breathing seen in the winter sleep of hibernating animals. Dur- 

 ing this condition, on account of the depression of metabolism less 2 

 is required' and less C0 2 is produced, so that the exchange of leases 

 through the pulmonary endothelium is greatly diminished. The dead 

 space, however, remains of the same capacity, which amounts to the 

 same thing as if the latter had been prolonged under unchanged con- 

 ditions of pulmonary gas exchange. 



