314 



THE NERVOUS REGULATION OF THE HEART 



its beat automatically whenever the stimulation is unduly prolonged. 

 It seems, therefore, that the excitation eventually induces a fatigue of 

 the inhibitor mechanism which permits the accelerator influences to 

 gain the upper hand. This "escape" of the organ from the power of 

 the vagus is generally confined to its ventricular portion, the auricles 

 remaining in the state of diastole. No definite statement can be made 

 regarding the length of time during which it is possible to maintain 

 the inhibition. In warm-blooded animals, the "inner stimulus" most 

 generally makes itself felt in the course of a few seconds, while in 



cold-blooded animals it does not 

 exert itself until after several min- 

 utes. To begin with, the heart 

 gives a few isolated beats, and then 

 gradually more until the normal 

 rhythm has again been established. 

 The inhibition is frequently 

 followed by an augmentor effect 

 which is characterized by an in- 

 " PH creased frequency, or strength of 

 contraction, or both. This second- 

 ary augmentation is especially well 

 shown in the frog, in which animal 

 the vagal and sympathetic fibers 

 are united into a common nerve at 

 some distance from the heart. For 

 this reason, the inhibitor as well 

 as the augmentor fibers are affected 

 whenever the trunk of the vagus 

 is stimulated. Their combined ex- 



rV-HB 



OH 



L, laryngeal; PH, SH, GH, OH, petro-, 

 sterno-, genio-, and omohyoid ; HG, hypo- 

 glossua; H, heart; BR, brachial plexus. 



FIG. 165. COURSE OF VAGUS NERVE IN 

 FROG. (Stirling.) 



SM, submentalis; LU, lung; V, vagus; 



GP, giosso-pharyngeal; HS, hypogiossai; citation, however, gives rise to an 



inhibition. If it is desired to stimu- 

 late the inhibitor fibers separately, 

 the electrodes must be applied to 

 them as they emerge from the vagal foramen and before they have 

 joined the sympathetic fibers. In explaining the fact that the ex- 

 citation of the combined vagosympathetic fibers always leads to an 

 inhibition, it must be remembered that the augmentation requires 

 stronger stimuli, possibly because the inhibitor mechanism is more 

 sensitive, or because the latent period of the augmentors is longer 

 than that of the inhibitors. Moreover, even if these impulses are 

 generated at precisely the same moment, as they probably are 

 when the vagus itself is stimulated, they cannot be pitted against 

 one another, because the augmentor influence cannot be made to 

 antagonize the inhibitor. Neither can the latter be made to counter- 

 act the former. It seems, therefore, that each impulse, when once 

 started, must run its course until the reaction to which it contributes 

 has been fully completed. Thus, as the inhibitor effect is produced 



