NERVOUS CONTROL OF THE BLOOD-VESSELS. 987 



lism of the tissues undergoes alteration, so that as a result of activity, e.y. in 

 muscles, lactic acid is formed instead of carbon dioxide. Lactic acid can 

 therefore be detected in the blood whenever violent exercise is taken sufficient 

 to produce dyspnoea, or 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 

 production of lactic acid. Lactic acid in- 

 troduced into the blood-stream, as is shown 

 in the curve in Fig. 455, B, is equally effica- 

 cious 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 ques- 

 tion in dealing with the regulation 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 FIG. 456. Tracing of arterial blood- 



\. /- pressure and of intestinal volume, 



on the blood- pressure curve caused by to show the influence of a moder- 



the heart-beats become very large. This ate increase in the C0 2 tension of 



J & the blood. (MATHISON.) 



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 comes 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- 

 inhibitory centre in the medulla probably partakes of the general excita- 

 tion 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. 



