NERVOUS CONTROL OF THE BLOOD-VESSELS 



985 



be concerned and which may influence the medullary centres and the heart. 

 When the renewal of the lung ventilation is stopped by ligature of the 

 trachea or by cessation of the respiratory movements, the increasing venosity 

 of the blood involves a diminished percentage of oxygen and an increased 

 percentage of carbon dioxide, and when asphyxia is excited by cessation 

 of the circulation through the medullary centres, these centres may suffer 

 at the same time from lack of oxygen and from the accumulation of carbon 

 dioxide. The question arises whether one or both of these factors are con- 

 cerned. It is easy to investigate the action of each separately. A pure 

 oxygen lack may be brought about by allowing an animal to breathe some 



A B 



t Resp.off -100 



-^20 



t 



on 



-ISO 



-100 



Nitrogen 



FIG. 454. Blood-pressure changes in a cat. A, after cessation of respiratory move- 

 ments. B, as a result of artificial respiration with nitrogen. (MATHISON.) 



inert gas, such as nitrogen or hydrogen, or in the curarised animal one of these 

 gases may be administered by the pump used for artificial respiration. The 

 effects of accumulation of carbon dioxide in the blood and tissues may be 

 produced by the administration of gaseous mixtures containing excess of 

 oxygen, i.e. 30 to 40 per cent., with varying percentages of carbon dioxide. 

 In the first case, the tension of the carbon dioxide in the blood will be kept 

 below normal ; in the second case, the tension of oxygen in the blood will 

 be kept above normal. In order to obtain results uncomplicated by the 

 influence of anaesthetics, the experiments may be carried out in animals 

 which have been deprived of consciousness by destruction of the brain above 

 the superior corpora quadrigemina. At different times physiologists have 

 been inclined to ascribe the excitatory phenomenon of 'asphyxia either to 

 absence of oxygen or to excess of carbon dioxide. Mathison has shown that 

 both conditions may concur in the production of the rise of blood-pressure 

 in asphyxia. In Figs. 454 and 455 the rise of arterial pressure produced by 



