THE CONTROL OF THE RESPIRATION 365 



phenomenal; in one individual, for example, after breathing forcibly for 

 a few minutes and then filling the lungs with 2 , apnea lasted for eight 

 minutes and seventeen seconds. 



The Supposed Nervous Element in Apnea 



It is necessary to point out that; prior to the elaboration of accurate 

 methods for the investigation of the chemistry of respiration, many 

 physiologists interpreted the apnea following forced breathing as the 

 result of a sort of inhibition, of the respiratory center brought about by 

 its repeated stimulation by afferent- nervous impulses transmitted to it 

 along the vagus nerves, these impulses being set up by the frequent col- 

 lapse and distention of the alveoli acting on the terminations of the 

 nerve. In justification of the nervous interpretation of apnea, it was 

 claimed by the earlier observers that it could not readily be produced 

 in animals after severing both vagus nerves. More recent work has 

 shown tha* this is not an accurate observation, for if the severing of 

 the vagi is accomplished not by cutting but by freezing, then apnea is 

 as readily produced as in an intact animal (Milroy). 28 



That chemical and not nervous factors cause the apnea is further 

 demonstrated by the well-known experiment of Fredericq, who, after 

 ligating the vertebral and one of the carotid arteries in two dogs, anas- 

 tomosed the central end of the remaining carotid of the one to the 

 peripheral end of the carotid of the other animal, thus establishing a 

 crossed circulation. He then found that by applying forced artificial 

 respiration to the one animal, the apnea which supervened affected the 

 other animal and not that to which the artificial respiration had 

 actually been applied. Another proof of the chemical theory of 

 apnea is furnished by the observation that if forced breathing is per- 

 formed in an atmosphere containing C0 2 in about the same partial pres- 

 sure as in the alveolar air, no apnea supervenes, and if the experiment 

 is repeated several times with progressively declining percentage of 

 C0 2 in the air each time, the length of the apneic pause proportionally 

 increases as the C0 2 pressure in the inspired air diminishes. 



Although in the foregoing account we have adopted Haldane's view 

 that oxygen deficiency per se can act as an excitant of the respiratory 

 center only when it is of extreme degree, it should nevertheless be pointed 

 out that studies by A. S. Loevenhart on the action of cyanides on the 

 respiratory center have led him to conclude that interference with oxida- 

 tive processes may be a more potent factor in its stimulation than the 

 experiments in which oxygen-poor atmospheres are respired would lead 

 us to expect. We must await further evidence before a final verdict is 

 pronounced on this most perplexing problem of modern physiology. 



