380 THE RESPIRATION 



Taking all these facts together, a strong case appeared to be made 

 for the acidosis hypothesis and this seemed to be almost established since 

 Haldane and his collaborators were apparently able to apply it in ex- 

 plaining the results of their numerous investigations of the respiratory 

 function. It will be observed, however, that all of the evidence is cir- 

 cumstantial in nature, and that the changes observed in anoxemia may 

 be due to entirely different causes. Lowering of the alkaline reserve of 

 the blood, lowering of the tension of C0 2 in the alveolar air, and hyperp- 

 nea can undoubtedly all result from deficiency of oxygen-supply to the 

 tissues, but the sequence in which the changes occur may be exactly the 

 opposite to that which is assumed in the acidosis hypothesis; it is pos- 

 sible, namely, that the deficiency in oxygen first excites the respiratory 

 center, the increased breathing then causes a blowing off of the free CO 2 

 from the blood, and the alkali is then excreted from the blood in the en- 

 deavor to hold C H at a constant level. If some method were available for 

 precise measurements of C H of the arterial blood at frequent intervals it 

 would be possible to settle this question once and for all, but such is not 

 the case, and we must seek for proof for the new hypothesis by indirect 

 means.* Assuming then that the respiratory center is excited by a slight 

 degree of anoxemia, let us see how the known facts fit in. The diminution 

 in oxygen in the blood excites the respiratory center and causes increased 

 breathing. This results in a blowing off of C0 2 from the blood into the al- 

 veolar air, so that there comes to be relatively more C0 2 excreted than 2 

 absorbed, and the respiratory quotient becomes raised. We have shown 

 this very clearly in experiments on decerebrated cats breathing in oxy- 

 gen-poor atmospheres; even when the oxygen percentage was only slightly 

 reduced, R.Q. had already risen to over unity. As a result of this blow- 

 ing-off of C0 2 , CH of the blood must tend to fall and this may explain 

 the tendency for the breathing to return towards the normal. It is impor- 

 tant for practical reasons to realize that when this condition becomes 

 established (i. e., slight anoxemia along with diminished CH, increased 

 breathing will not compensate for the anoxemia, for the advantage gained 

 by higher saturation of the blood with oxygen is counteracted by the al- 

 kalosis produced because the oxygen-carrying power of the hemoglobin has 

 become altered. Under such conditions as pointed out on page 401 the 

 hemoglobin holds on more tightly to the oxygen and does not give it up to 

 the tissues. Under these conditions neither increased breathing nor in- 

 creased bloodflow can force more oxygen into the tissues, so that both 

 the respirations and the pulse become less rapid after the initial accel- 

 eration. It is this prolonged anoxemia that causes the symptoms of 



*It may be stated, however, that Cn of the blood of man after he has been for some time in 

 rarefied air is still normal as judged by determination of the dissociation curve of his blood (page 

 402) in a partial pressure of COo equal to that of his alveolar air (Barcroft). This result shows 

 at least that the acid-base equilibrium is ultimately restored under the altered conditions. 



