THE NERVOUS CONTROL OF THE BLOOD VESSELS 1027 



interferes with the gaseous exchanges of the centre, whether obstruction to 

 respiration, absence of oxygen in the air breathed, or a failure of the blood 

 supply as by ligature of the cerebral arteries, calls forth an increased state 

 of activity of the centre. This can be best studied by observing the changes 

 in the blood pressure produced in a curarised animal by the cessation of 

 artificial respiration. 



These changes depend partly on the stimulation of the vaso-motor and 

 vagus centres by the venous blood, and partly on the affection of the heart 

 itself. We will first consider them with both vagi cut, in order to shut 

 out the action of the vagus centre. The blood pressure is registered by 

 means of a mercurial manometer in connection with the carotid artery. 

 On leaving of? the artificial respiration, the blood pressure may remain 

 at the same height for some seconds, the only change noticed being the 

 absence of the respiratory oscillations. Sooner or later the blood pressure 

 suddenly rises rapidly (Fig. 463, A), and in another ten seconds may 

 reach a height twice as great as it was previously. The heart beats a little 

 more forcibly in consequence of the increased cardiac tension, but i|s fre- 

 quency is almost unaltered. The blood pressure remains at this height 

 for about a minute and then gradually falls, the heart beats becoming 

 smaller and smaller until the pressure has sunk to a point very little above 

 the abscissa line (level of no pressure). This fall in pressure is due to the 

 failure of the heart. The heart, badly supplied with oxygen, cannot overcome 

 the high resistance presented by the contracted arterioles ; it gets overfilled, 

 and gradually loses the power of expelling any of its contents. If, when the 

 blood pressure has sunk to its lowest point, the heart be rapidly cut out of the 

 body, it will begin to beat fairly forcibly, being relieved of the excessive 

 internal tension. The vessels however remain constricted until the death 

 of the animal. This is shown by two facts. If, while the pressure is sinking, 

 artificial respiration be recommenced, the heart supplied with oxygen at once 

 begins to beat more forcibly, and the blood pressure may rise to an even 

 greater height than immediately after the commencement of the asphyxia. 

 Again, if the volume of the kidney be recorded by means of the oncometer, 

 the rise of general blood pressure produced by asphyxia is seen to be accom- 

 panied by a marked shrinking of the kidney, and this shrinking endures until 

 the animal dies, showing that the fall of blood pressure following the rise 

 is due, not to a giving way of the arterial resistance, but to failure of the 

 heart. 



Similar results are obtained when the vessels to the brain are ligatured, 

 or when the animal has to respire an indifferent gas free from oxygen, such 

 as nitrogen (Fig. 463, B) or hydrogen. In the uncurarised animal the rise 

 of blood pressure is associated with increased respiratory movements and 

 finally with convulsive spasms which may involve practically every muscle 

 of the body. 



We have spoken above of the phenomena of asphyxia as being due to 

 the circulation of venous blood. There are however two factors which may 

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



