636 APNGEA. [BOOK n. 



was the result of too great, just as dyspnoea is the result of too 

 little arterialization of the blood reaching the respiratory centre. 

 It was argued that owing to the increased vigour of the artificial 

 respiratory movements the hsemoglobin of the arterial blood, 

 which in normal breathing is not quite saturated with oxygen, 

 became almost completely so, and that at the same time the 

 quantity of oxygen simply dissolved in the blood became largely 

 increased and its pressure largely augmented. But there are 

 reasons which render such a view untenable. In the first place 

 there is no direct and satisfactory proof that in apnoea the arterial 

 blood is overloaded with oxygen as supposed; indeed during the 

 course of apnoea before it has come to an end the blood becomes 

 distinctly less arterial, more venous than usual. In the second 

 place apnoea if not entirely impossible, is much more difficult to 

 bring about when both vagus nerves are divided, and if it does 

 occur after section of the vagus nerves has not the same characters 

 as ordinary apnoea. Now, when artificial respiration is being 

 carried on, section of the vagus nerves can have no effect on the 

 quantity of oxygen taken up by the blood in the lungs. But 

 the vagus nerves are the channel of impulses affecting the 

 respiratory centre, and this relation of the apnoea to the vagus 

 nerves suggests another and different interpretation of apnoea. 

 As we have seen, expansion of the lung by acting in some way 

 or other on the pulmonary terminations of the vagus nerve 

 sends up along that nerve impulses which inhibit inspiration. 

 And it is argued that repeated forcible inflations of the lungs 

 produce apnoea by generating potent inhibitory impulses, which 

 by a kind of summation of their effects in the bulb stop for 

 a while the generation of respiratory impulses in the respiratory 

 centre. This conclusion moreover is strongly supported by the 

 fact that an apnoea may be produced, so long as the vagus 

 nerves are intact, by forcible artificial respiration with hydrogen 

 instead of atmospheric air; in other words, the inhibitory im- 

 pulses generated in the vagus nerves by the inflation are 

 sufficient wholly to neutralize the development of respiratory 

 impulses which the deficient arterialization of the blood would 

 otherwise have produced. The exact nature and development 

 of such a summation of inhibitory impulses, especially in the 

 presence of correlative augmentative impulses called forth by the 

 corresponding successive collapses of the lungs, is too complex a 

 matter to be dwelt on here. Moreover an apnoea may be produced 

 though, as we have said, with difficulty after section of both vagus 

 nerves ; but in this case air and not hydrogen must be used for 

 inflation, the use of the latter, in contrast to the result when the 

 nerves are intact, leading to dyspnoea. The subject cannot as 

 yet be considered as fully cleared up. That apnoea as ordinarily 

 produced is in some way the result of inhibitory impulses gene- 

 rated by the inflations can however hardly be doubted. 



