NERVOUS CONTROL OF THE BLOOD-VESSELS 1109 



when the access of oxygen is diminished by poisoning with carbon 

 monoxide, or by reducing the tension of this gas in the air breathed. 

 Oxygen lack can be regarded therefore as synonymous with the pro- 

 duction of lactic acid. Lactic acid introduced into the blood-stream, 

 as is shown in the curve in Fig. 458, B, is equally efficacious with 

 oxygen lack or with carbon dioxide excess in the production of a rise 

 of blood pressure indistinguishable from the asphyxial rise. It seems 

 therefore that the common factor in asphyxia is the increased acidity 

 or H' ion concentration of the blood. We shall have occasion to 

 return to this question in dealing with the origin of the respiratory 

 movements. 



If in the dog, and to a less extent in other animals, the vagi be 

 left intact, the blood-pressure tracing during asphyxia has quite 

 another appearance. At the point of the tracing corresponding to the 

 rapid rise in the previous experiment there is in this case only a slight 

 rise of pressure, but the heart begins to beat very slowly. At each 

 beat it necessarily sends out a greater volume of blood than when it 

 is beating more frequently, and hence the oscillations on the blood- 

 pressure curve caused by the heart-beats become very large. This 

 slow beat is due to the action of the vagus centre, and is at once 

 abolished by section of the two vagi. The sparing of the heart by 

 means of this vagus action enables it to last longer, and the final fatal 

 fall of blood pressure due to heart failure conies on rather later than 

 when the vagi are divided, in the increased vagus action which occurs 

 during asphyxia two factors are probably involved. The cardio-inhibi- 

 tory centre in the medulla, probably partakes of the general excitation 

 of the medullary centres due in the first place to carbon dioxide excess, 

 in the second to oxygen lack. More important is the direct action of the 

 rise of blood- pressure on the medullary centre. The rise of arterial 

 pressure causes increased intracranial tension, and any increase of the 

 latter excites the vagus centre and produces slowing of the pulse. The 

 vagus slowing is therefore absent in asphyxia if the arterial blood be 

 allowed to escape through a mercury valve so as to prevent any rise 

 of pressure in the brain cavity. 



During the period of increased pressure waves are often observed 

 on the blood-pressure curve. These are of two kinds. In the first 

 place, in completely curarised animals we may observe oscillations of 

 blood pressure corresponding with the respiratory rhythm before 

 the administration of curare, or if the vagi are cut, presenting a 

 rhythm similar to that usual in animals with divided vagi. These 

 waves are known as the Traube-Hering curves from the physiologists 

 by whom they were first observed. They are certainly due to irradia- 

 tion of impulses from the excited respiratory centre to the vaso-motor 

 centre in the medulla. In fact, if the curarisation is not complete, a 



