468 Dr. J. A. Mac William. Influence of the Central [May 18, 



stimulation of the local inhibitory mechanism of the heart. For the 

 administration of atropin in doses sufficient to paralyse that mechan- 

 ism does not obviate the slowing effect of the anaesthetic. (The 

 paralysed condition of the inhibitory mechanism was verified by 

 strong electrical stimulation of the inhibitory area, described in 

 former papers in the ' Proceedings of the Royal Society,' vol. 44, 

 and the ' Journal of Physiology,' vol. 9, 1888.) 



From these results it appears that chloroform acts on the heart, 

 and distinctly slows its rate of beat through a depressing or retarding 

 influence exerted on the intrinsic rhythmic mechanism of the organ. 



Further, it is evident that the reduction in the pulse rate that 

 occurs in the second stage (B) of chloroform anaesthesia is of a two- 

 fold origin : it partly results from the action of chloroform on the 

 heart itself, but it very largely depends on the integrity of the vagi. 

 The vagus centre in the medulla, though rendered incapable of reflex 

 excitation, is not paralysed even during deep anaesthesia ; it con- 

 tinues, as a rule, to exert a very important controlling influence upon 

 the cardiac rhythm, and it is indeed to the exercise of this controlling 

 influence that the reduction of the pulse rate from the excessively 

 high rapidity often present during the stage of acceleration is mainly 

 due. Even during profound anaesthesia, section of the vagi leads, as 

 a rule, to a striking acceleration of the pulse rate, though the rapidity 

 does not become as great as during a lighter anaesthesia. When the 

 anaesthesia is allowed to become less deep the rate of heart beat 

 increases decidedly. 



As regards the notable acceleration of the heart which occurs in 

 the first stage (A) of chloroform administration (stage of excitement), 

 this is not to be accounted for by an assumed excitation of the cardiac 

 augmentor nerves, for marked acceleration occurs under the influence 

 of the anaesthetic even when the augmentor nerves have been excluded 

 by section. 



On the other hand, the action of chloroform at different stages of 

 its administration on the heart itself after section of all the cardiac 

 nerves shows no ground for assuming that the acceleration might be 

 due to direct influence on the intrinsic rhythmic mechanism. 



Moreover, the general indications of excitement in the central 

 nervous system (respiratory centre, &c.) point to the probable occur- 

 rence of central changes in the centres of the regulating nerves. 

 And as an assumed activity of the augmentor nerves has been set 

 aside as inadequate to meet the facts, there remain only the vagi. A 

 reduction in the controlling influence of the vagus centre would cause 

 such an acceleration as that which usually occurs, and it is, I believe, 

 to such a change that the quickened pulse rate is mainly, if not 

 entirely, due. 



This change — the diminution in activity of the vagus centre — is 



