RELATION OF RESPIRATION TO THE NERVOUS SYSTEM 283 



the rate and the depth of respiration are increased, in the vagoto- 

 mized 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 ulti- 

 mately 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 exag- 

 geration of breathing the terms Hyperpncea and Dyspnoea have been 

 respectively applied. If the gaseous interchange remains insuffi- 

 cient, 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-dyspncea.) (p. 32). 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. 



Apncea. The physiological opposite of dyspnoea is apncei. This 

 condition may be produced in an animal by rapid or prolonged 

 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 respiration 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 apnosa 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 themselves (expiratory apnoea), but in the inspiratory 

 phase if they have been emptied by suction and then permitted of 

 themselves to expand (inspiratory apnosa). The apnoea is not pro- 

 duced, as some have thought, by the accumulation of an excess of 

 oxygen in the blood, for rapid and repeated inflation of the lungs 

 with hydrogen may cause the condition. Indeed, towards the end 

 of the apnosic period the venous blood may be very distinctly poorer 

 in oxygen than normal venous blood. Apnoea is easily caused in 

 man by a period of deep and rapid breathing and in other ways. 

 The essential thing in this chemical or true apnoea (apncea vera) 

 is the lowering of the partial pressure of carbon dioxide in the 

 alveolar air, and therefore in the arterial blood and the respiratory 



