THE NERVOUS REGULATION OF THE HEART 163 



together through the inferior cervical ganglion. Upon opening this 

 sheath they may with care be separated, the fibres running in distinct 

 strands, and not mixed together as in the vago-sympathetic oi the frog. 

 For some distance below the superior cervical ganglion the cervical 

 sympathetic is not connected with the vagus, and here the nerves may 

 be separately stimulated without any artificial isolation. In the rabbit 

 and some other mammals, including man, the vagus and sympathetic 

 run a separate course in the neck. 



In the mammal, the inhibitory fibres have a smaller direct action 

 on the ventricle than in the frog. It indeed beats more slowly when 

 the auricle is slowed, but this is only because in the normally beating 

 heart the ventricle takes the time from the auricle. The strength 

 of the ventricular contractions may be not at all diminished, even 

 when the auricle is beating very feebly during inhibition. When the 

 auricle is completely stopped, which does not occur so readily as in 

 the frog, the ventricle also stops for a short time, but soon begins to 

 beat again with an independent rhythm of its own. In the frog the 

 ventricle is directly affected by stimulation of the vagus, and the 

 force of its beats is diminished independently of the inhibitory 

 effects in the auricles (Practical Exercises, pp. 198, 203). 



It has been shown by delicate optical methods of recording the 

 contraction of small units of the auricular musculature (designated 

 as the ' fractionate ' contraction by Wiggers) by the method illus- 

 trated in Fig. 736, that the diminution in the size of the contrac- 

 tion produced by stimulation of the vagus is essentially due to 

 depression of the contractility of the muscle, and not, or at any rate 

 not primarily, to a diminution in its excitability. In other words, 

 the strength of stimulus needed to elicit a contraction of the muscle 

 when under the influence of vagus excitation, in the early part of 

 the inhibition at least, is not increased, whereas the size of the 

 contraction evoked by a given stimulus is diminished (Fig. 74) . 



It is not doubted that the excitation of the vagus does reduce the 

 excitability of the auricular muscle, but this reduction seems not to 

 occur so early as the reduction in the amplitude of the beat, and 

 cannot therefore be responsible for it. The duration of each 

 (fractionate) contraction is not altered by vagus excitation. It 

 can likewise be shown that the depression of contractility is not 

 secondary to the depression of conductivity produced by the vagus. 

 Finally, it is not dependent upon the slowing of the rhythm which 

 accompanies the diminution in the contraction of the naturally 

 beating auricle. For when the auricle is compelled to beat with an 

 artificial rhythm by applying to it a series of regularly spaced 

 electrical stimuli at a more rapid rate than the normal rhythm, 

 stimulation of the vagus still causes reduction in the amplitude of 

 the contraction without change in the rate (Fig. 74). One other 

 point is worthy of note. Excitation of the vagus causes an increase 

 in the size of the first, or occasionally of the first two subsequent 



