302 ATROPIN AND MUSCARIN. [BOOK i. 



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 pro- 

 found. 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. 

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

 many other respects) the antidote of the other. And, as in the 

 case of atropin, so in the case of muscarin, there is evidence that 

 the drug acts not on any ganglionic mechanisms but on the cardiac 

 tissue itself. 



The conclusion that inhibition is the result of changes in the 

 cardiac tissue itself may serve to explain why in inhibition sometimes 

 the slowing sometimes the weakening is the more prominent. When 

 the inhibitory impulses, by reason of particular fibres being affected 

 or otherwise, are brought to bear chiefly on those parts of the heart, 

 such as the sinus, which possessing higher rhythmic potentiality 

 (see 156) determine the sequence and set the rate of rhythm, it 

 is the rate which is most markedly affected. When on the other 

 hand the inhibitory impulses fall chiefly on the parts possessing 

 lower rhythmic potentiality, the most marked effect is a diminution 

 in the force of the contractions. 



There is no adequate evidence then that the cardiac ganglia 

 act as an inhibitory mechanism in the sense that they pro- 

 duce important changes in the nature of the impulses reaching 

 them along vagus inhibitory fibres before those impulses pass on 

 to the muscular tissue. We may add that there is similarly no 

 adequate evidence that any of the ganglia act as an ' augmenting ' 

 mechanism. We have previously seen, 155, 156, reasons for 

 thinking the ganglia are not centres for the origination or 

 regulation of the spontaneous beats. The question then arises, 

 What are their functions ? To this question we cannot at present 

 give a wholly satisfactory answer. 



The inhibitory fibres remain as we have seen medullated 

 fibres until they reach the heart, but it would appear that they 

 lose their medulla, somewhere, in the heart before they actually 

 reach the muscular tissue, and it is probable that the loss 

 takes place in connection with some of the cardiac ganglia 

 much in the same way that the augmenting fibres lose their 

 medulla in the ganglia of the sympathetic chain ; but we do 

 not know what is the physiological effect or the purpose of this 

 loss of the medulla, and we cannot suppose that this is the sole 

 or even chief use of the ganglia. Coincident with the loss of the 

 medulla an increase of fibres frequently takes place, more than 

 one non-medullated fibre leaving a nerve cell into which one 

 medullated fibre enters ; and we may suppose that this mode of 

 branching has purposes not fulfilled by the mere division of a 

 fibre. Then again bearing in mind the nutritive or "trophic" 



