392 



Prof. W. M. Bayliss. 



The rate of blood flow through the limb was recorded by an electrical drop 

 recorder. 



It has been already mentioned that, after blood has been removed, the 

 arterial pressure rises again fairly rapidly to a certain degree, independently 

 of the injection of any fluid. This rise appears to be too rapid to be 

 accounted for, at all events in its initial stage, by absorption of fluid from the 

 tissues. Indeed, 1 was unable to obtain evidence of dilution of the blood 

 within 3 niins., although the arterial pressure had risen from 38 mm. of 

 mercury to 66 mm. When the circulation through the perfused limb was 

 observed during this period, there was seen to be a progressive slowing of the 

 rate of flow, this slowing was replaced by an increased rate when injections 

 of gum solutions were made into the jugular vein of the animal itself. The 

 results of Pilcher and Sollmaun were thus confirmed. It was noticed also, as 

 would be expected, that the first stage of asphyxia was accompanied by a 

 slowing of the circulation through the limb. The constriction passed off in 

 the later stages, as the nerve centres become paralysed. 



We see now why it was found in some cases that injection of gum solution, 

 of equal volume and viscosity to that of the blood removed, caused a 

 temporary rise of arterial pressure above that existing before the loss of 

 blood. The injection was made into a system in which the arterioles were to 

 some extent constricted by impulses from' nerve centres. 



The cause of the peripheral vaso-dilatation produced by rise of arterial 

 pressure seems clear. The depressor nerves were intact, and a sufficient 

 explanation is afforded by stimulation of their receptor endings in the aorta 

 or heart. The peripheral vaso-eonstriction produced by fall of pressure is 

 not quite so simply explained. Pilcher and Sollmaun are inclined to attribute 

 it to anaemia of the vaso-constrictor centre. The result of this is presumably 

 a greater or less accumulation of carbon dioxide, not sufficiently rapidly 

 removed by the blood current, and it has been shown that carbon dioxide 

 excites nerve centres. I do not altogether understand whether these authors 

 regard this as the cause. They state that they have excluded asphyxial 

 effects by the insufflation of oxygen. But it does not follow that more 

 oxygen is actually supplied to the nerve centres, since the blood may have 

 been practically saturated already, and the rate of blood flow is not 

 necessarily increased. There may, therefore, have been a slight rise in the 

 carbon dioxide content of the centres, even when oxygen is insufflated into 

 the lungs. The comparatively slow rate of onset of the vaso-eonstriction in 

 my experiments is in favour of this explanation. A brief stimulation of 

 the vagus nerve, so that the heart was stopped, did not result in any 

 detectable change in the rate of flow through the limb. 



