176 SECTIONAL ADDRESSES 



sarily rise, presumably because there has been a compensatory dilatation 

 of vessels in the rest of the animal. A number of workers, especially 

 Fleisch, have demonstrated that vessels are sensitive to most minute changes 

 of hydrogen -ion concentration, even that which is produced by the addition 

 of the normal amount of carbon dioxide to the blood, and personally I 

 think that normally this is the most important factor concerned. 



There is, however, evidence that certain substances of protein origin 

 may be involved. Of these the most important is histamine. It has 

 recently been shown by Anrep that the vasodilator substance which is 

 liberated into the venous blood gives all the known biological reactions for 

 histamine, and it is possible to demonstrate that extensive tetanisation of 

 muscles may produce a state which is a very similar one to histamine 

 shock. There is at the same time a constriction of pulmonary vessels 

 such as is produced by histamine. This liberation of histamine — if it be 

 histamine — is of interest, as biochemists have reported that, compared with 

 other tissues, muscles contain relatively little histamine. It is, however, 

 somewhat doubtful if we are justified in considering that what happens 

 during a severe artificial tetanus necessarily occurs in normal exercise. 



It has been suggested also that other substances of protein origin, such 

 as adenylic acid, may be concerned. Whatever the agent it seems likely 

 that some metabolic products are responsible, if not for the dilatation 

 during exercise, certainly for the continued dilatation which continues 

 after the exercise. 



The nervous dilatation is, judging from the work of Cannon and his 

 associates, probably sympathetic. Here we see a dual function of the 

 sympathetic, for its constrictor action is much better known. It has been 

 known for some time that the sympathetic contained vasodilator fibres. 

 Indeed, Dastre, a successor of Claude Bernard, states that, had Bernard 

 chanced to use a dog instead of a rabbit for his classical experiments on 

 the sympathetic, he would have been more impressed with its vaso- 

 dilator than with its now much better known vasoconstrictor action. 

 In order to show the vasodilator fibres in the sympathetic, it is necessary 

 to paralyse first the vasoconstrictor fibres with ergotoxine (Dale), or to 

 use slow rates of stimulation. In this connection it may be remarked 

 that this slow rate of stimulation may be an imitation of what normally 

 occurs, since presumably ordinary muscle contraction may give rise to 

 similar stimuli. It is interesting to note that the dilator action is easily 

 shown in the dog, but it has not been possible to show it in the cat ; but 

 the exact significance of the point is unknown. 



Once the exercise has begun it seems likely that local vasodilator 

 reflexes, similar to Loven reflexes, are set up by afferent impulses arising 

 within the muscles themselves, possibly as a result of the mechanical and 

 chemical changes which take place. The evidence is somewhat scanty, 

 but it is impossible to ignore any longer the possibility of the existence of 

 a nutrition reflex as suggested by Hess and supported more recently by 

 Fleisch. By this is meant the fact that oxygen lack in a part sets up afferent 

 impulses which result in reflex dilatation. 



Capacity effects. — Now it has been shown by Krogh that when a muscle 

 is active an enormous number of hitherto closed capillaries open up. 

 The best evidence of this is probably his well-known Indian ink experiment. 



