300 INHIBITORY AND AUGMENTOR FIBRES. [BOOK i. 



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. 



The anterior roots of the second and third dorsal nerves, and 

 the (white) rami communicantes belonging to them, which, as we 

 have just seen, contain in the dog augmentor fibres, also consist 

 exclusively of medullated fibres. But the nerves which convey 

 the augmenting impulses from the lower cervical ganglion or 

 from the annulus of Vieussens to the heart consist of non- 

 medullated fibres. Hence the augmentor fibres must have lost 

 their medulla and become continuous with non-medullated fibres 

 somewhere in their course along the sympathetic chain. It is 

 probable that the change occurs in the ganglion stellatum and 

 lower cervical ganglion, and it is further probable that the change 

 is effected by the medullated fibre passing into one of the ganglion 

 cells, and so losing its medulla, the impulses which it conveys 

 passing out of the nerve cell by one or more of the other 

 processes of the cell which are continued on as non-medullated 

 fibres. Of. 98. 



In the dog then these two sets of nerve fibres, antagonistic to 

 each other in function, differ in structure, the augmentor fibres 

 early losing their medulla and hence being over a large part of 

 their course non-medullated fibres, whereas the inhibitory fibres 

 are medullated fibres, which though they may pass by or through 

 ganglia (as the ganglion jugulare and ganglion trunci vagi) do not 

 lose their medulla in these ganglia but remain as medullated 

 fibres right down to the heart. And this difference in structure 

 appears to hold good for all mammals, and is possibly true for 

 vertebrates generally. 



161. The question, What is the exact nature of the change 

 brought about by the inhibitory and augmenting impulses re- 

 spectively on their arrival at the heart ? or, in other words, By 

 virtue of what events produced in the heart itself do the impulses 

 of one kind bring about inhibition, of the other kind augmentation ? 

 is a very difficult one, which we cannot attempt to discuss fully 

 here. We may if we please speak of an u inhibitory mechanism " 

 placed in the heart itself, but we have no exact knowledge of the 

 nature of such a mechanism. Still less do we possess any satisfactory 

 information as to an augmenting mechanism. It has been suggested 

 that some of the ganglia in the heart serve as such an inhibitory 

 (or augmenting) mechanism ; but there is evidence that the 

 inhibitory impulses produce their effect by acting directly on the 

 muscular fibres, or at all events do not produce their effect by 

 acting exclusively on any ganglia. One evidence of this kind is 

 supplied by the action of the drug atropin. 



If, either in a frog or a mammal, or other animal, after the 

 vagus fibres have been proved, by trial, to produce, upon stimu- 

 lation, the usual inhibitory effects, a small quantity of atropin 



