CHAP, iv.] THE VASCULAR MECHANISM. 319 



dose of atropin, the strongest stimulation of the vagus will not 

 produce standstill or appreciable slowing or weakening of the beat. 

 Further, this special action of atropin on the heart is so to 

 speak complemented by the action of muscarin, the active 

 principle of many poisonous mushrooms. If a small quantity of 

 muscarin be introduced into the circulation, or applied directly to 

 the heart, the beats become slow and feeble, and if the dose be 

 adequate the heart is brought to a complete standstill. The effect 

 is in some respects like that of powerful stimulation of the vagus, 

 but the standstill is much more complete, the effect is much more 

 profound. Now if, in a frog, the heart be brought to a standstill 

 by a dose of muscarin, the application of an adequate quantity of 

 atropin will bring back the beats to quite their normal strength and 

 rhythm. The one drug is so far as the heart is concerned (and indeed 

 in many other respects) the antidote of the other. We may interpret 

 these results as indicating that there exists in the heart an 

 inhibitory mechanism, which is excited, stimulated into activity 

 by muscarin, but paralysed, rendered incapable of activity by 

 atropin. And we may suppose that there is a corresponding 

 augmenting mechanism. 



But what is the nature of such a mechanism? It has been 

 supposed that it is furnished by some or other of the ganglia 

 within the heart. And this view seems at first sight tempting, 

 especially as regards the vagus inhibitory fibres. In the dog the 

 roots of the spinal accessory nerve, by which inhibitory fibres leave 

 the central nervous system, consist entirely of medullated fibres. 

 Among these are fibres of fine calibre, 3'o/jt, or less in diameter, 

 which may be traced down the trunk of the vagus, along the 

 branches going to the heart, right down to the heart itself. There 

 can be little doubt that these medullated fibres of fine calibre are 

 the inhibitory fibres of the vagus, and" indeed there is evidence 

 which renders it probable that the inhibitory fibres of the heart 

 are always medullated fibres of fine calibre, which continue as 

 medullated fibres right down to the heart but eventually lose their 

 medulla in the heart itself by becoming connected with the cells 

 of some or other of the ganglia. And we may suppose that the 

 impulses passing down the vagus fibres so affect the cells 

 with which the fibres are thus connected, that the impulses 

 which pass away from the other side of the cell towards 

 the muscular fibres assume a special character and become 

 inhibitory, whatever might have been their nature before. In other 

 words these gauglionic cells are the inhibitory mechanism of which 

 we are in search. But the connection of a fibre with a nerve cell and 

 a change from a medullated to a non-medullated condition does not 

 necessarily entail change of function. The augmentor fibres as they 

 leave the spinal cord by the anterior roots of the thoracic spinal 

 nerves are medullated fibres. But they lose their medulla (in the dog) 

 in the stellate ganglion or the lower cervical ganglion ; from these 



