RESPIRATION 231 



chemical regulation (through the carbon dioxide) of the amount of 

 air moved into and out of the lungs per unit of time ; and a nervous 

 regulation (chiefly through the vagi) of the rate and depth of the 

 movements necessary to effect the given amount of ventilation. 



When the vagi have been divided, an increase in the carbon 

 dioxide pressure within certain limits is responded to by an 

 increase in the total ventilation, just as in the normal animal, 

 but the form of the response is different. Whereas in the normal 

 animal both the rate and the depth of respiration are increased, 

 in the vagotomized animal there is a marked increase in depth, 

 with little or no increase in rate (Scott). 



When the gaseous exchange in the lungs from any cause 

 becomes insufficient, the respiratory movements are exaggerated, 

 and ultimately every muscle which can directly or indirectly 

 act upon the chest-wall is called into play in the struggle to pass 

 more air into and out of the lungs. To a lesser and greater 

 degree of this exaggeration of breathing the terms Hyperpnoea 

 and Dyspncea have been respectively applied. If the gaseous 

 interchange remains insufficient, or is altogether prevented, 

 asphyxia sets in. Sometimes in man impending asphyxia from 

 loss of function by a part of the lungs (with crippling of the lesser 

 circulation) , as in pneumonia, may be warded off by inhalations of 

 oxygen. Increase in the temperature of the blood circulating 

 through the spinal bulb, as when the carotid arteries of a dog are 

 laid on metal boxes through which hot water is kept flowing, also 

 causes dyspnoea (heat-dyspnoea) (p. 290) . But if the temperature be 

 too high, the respiratory movements may be slowed, perhaps by 

 a partial paralysis or inhibition of the respiratory centre. When 

 the blood is cooled the respiration becomes deeper and slower, 

 but if the temperature is greatly and suddenly lowered, the 

 centre may be stimulated and the breathing quickened. In man 

 the increased temperature of the blood in fever is a cause, though 

 not the only one, of the increase in the rate of respiration. 



Apnoea. The physiological opposite of dyspnoea is apncea. 

 This condition may be produced in an animal by rapid or pro- 

 longed artificial respiration. It is especially easy to obtain in an 

 animal in which the circulation through the brain and bulb is 

 interrupted for a time and then restored, while artificial respira- 

 tion is being kept up. Spontaneous respiration returns after a 

 longer or shorter interval, but if the artificial respiration be still 

 maintained, it again ceases. In a successful experiment the 

 animal remains without breathing for many seconds after the 

 artificial respiration is stopped. In apncea the chest remains at 

 rest in the expiratory phase if the lungs have been inflated by 

 the artificial respiration and then allowed to collapse of them- 

 selves (expiratory apncea), but in the inspiratory phase if they 



