NERVOUS MECHANISM OF RESPIRATION. 341 



influenced by a deficiency of oxygen. Experimentally it can be 

 shown that the effect is produced, in a great measure at least, in 

 the medulla itself, by the blood flowing through it, and not by 

 the action of the venous blood circulating through distant organs, 

 and reflexly affecting the centre. It has also been shown that 

 the temperature of the blood circulating through the medulla 

 changes the activity of the centre, for, if the blood in the carotids 

 be warmed, the respiratory movements become more rapid. 



The respiratory centre is, then, a good example of what is 

 called an " automatic nerve centre," not depending upon nerve 

 impulses from afar for its energy, nor merely reflecting the in- 

 fluences of other centres, but acquiring its energy from the ther- 

 mal and chemical condition of the blood which flows through it, 

 and thus its activity is intimately related to its nutrition and sup- 

 ply of oxygen. 



So long as the amount of oxygen flowing through the centre 

 keeps up to a certain standard, the normal excitability of the 

 centre continues, and we have natural quiet breathing, called 

 JEupnoBa. When the oxygen falls below the normal standard the 

 respiratory centre becomes more excitable, and labored breathing 

 is produced, commonly called Dyspnoea. 



If the theory that a deficiency of oxygen is the normal stimulus 

 to action of the respiratory centre be correct, a superabundant 

 quantity should diminish the activity of the centre, and a con- 

 dition the opposite of dyspnoea would be produced. This is dif- 

 ficult to show in natural breathing, though every one knows the 

 efficiency of the few deep breaths one takes before a dive into 

 water ; but with artificial breathing, if the movements be carried 

 on very energetically for some time, and then be stopped, the 

 animal will not at first attempt to breathe, but after a short time, 

 somewhat less than a minute, gentle and slow respiratory move- 

 ments commence. This cessation of breathing, called apncea, de- 

 pends upon the blood being so charged with oxygen that it no 

 longer acts as a stimulus to the centre. 



We find that dyspnoea is produced by a deficiency in the 

 amount of oxygen rather than by an excess of carbonic acid gas. 

 This is proved by the fact that it occurs when the carbonic acid 



