INNERVATION OF THE RESPIRATORY MOVEMENTS. 625 



presence of C0 2 , it follows logically that the more complete removal 

 of this gas by ventilation of the lungs should be considered as the 

 chief cause of true apnea. Experimentally this view is well 

 borne out by an old observation of Berns, according to which a 

 condition of apnea in a rabbit may be cut short instantly at any 

 moment by a blast of C0 2 sent into the lungs, a blast of air having 

 no such affect. This observation is further supported by recent 

 experiments by Mosso* upon men, in which he shows that apnea 

 can not be produced by inflation with carbon dioxid. This author 

 designates the condition of diminished C0 2 in the blood as acapnia. 

 According to this terminology, true apnea is due to a condition of 

 acapnia. 



In the intact animal, therefore, we may say that apnea is 

 due to two causes: first, the removal of C0 2 from the blood by 

 better ventilation, whereby the center is stimulated less strongly 

 or not at all; and, second, the rhythmical inhibition of the center 

 through the vagus fibers ending in the lungs. The two causes work 

 together, and, as it were, aid each other, for, the less the irritability 

 of the center, the more easily it is inhibited, and, the more it is 

 inhibited, the less the internal stimulus affects it. 



Innervation of the Bronchial Musculature. Numerous 

 investigators, using different methods, have demonstrated that the 

 bronchial musculature is supplied through the vagus with motor 

 and inhibitory fibers, bronchoconstrictor and bronchodilator fibers, 

 as they are usually called. t Stimulation of the constrictors causes 

 a narrowing of the bronchi, and therefore increases the resistance to 

 the inflow and outflow of air. Some observers state that these fibers 

 are normally in a condition of tonic activity (Roy and Brown), 

 but others find little evidence for this belief. An artificial tonus 

 that is, a condition of maintained activity of the constrictor fibers 

 may be set up by the action of a number of drugs, such as muscarin, 

 pilocarpin, and physostigmin, which in this case, as in so many 

 other instances of autonomic fibers, are supposed to stimulate the 

 endings of the fibers in the lungs. Their effect is removed by the 

 action of atropin. These fibers are stimulated also during the ex- 

 citatory stages of asphyxia. Reflex stimulation of the constrictors 

 is obtained most readily (Dixon and Brodie) by irritation of the 

 nasal mucous membrane, and it seems probable that in bronchial 

 or spasmodic asthma these fibers are also stimulated reflexly. 



The normal conditions under which the constrictors and dilators 

 are brought into play can scarcely be stated. Irritating vapors or 

 even C0 2 lead to a bronchoconstriction and this reflex, as stated on 



* Mosso, "Archives italiennes de biologie," 40, 1, 1903. 

 t For a recent paper with references to literature see Dixon and Brodie, 

 "Journal of Physiology," 29, 97, 1903. 

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