A reversed action of the vagus on the mammalian heart / by H.H. Dale, P.P. Laidlaw, and C.T. Symons.

  • Henry Hallett Dale
Date:
[1910?]
Catalogue details

Licence: Public Domain Mark

Credit: A reversed action of the vagus on the mammalian heart / by H.H. Dale, P.P. Laidlaw, and C.T. Symons. Source: Wellcome Collection.

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    for 12 days subsequent to the second operation. It is clear, therefore, that fibres of the true sympathetic system can play no part in the production of the effect. The accelerator effect being thus undoubtedly due to fibres belonging to the vagus itself, we have a further choice of possibilities to consider. In the first place, it is conceivable that an actual reversal of function takes place under the influence of the drug, fibres which are normally inhibitor becoming accelerator under the abnormal conditions of the experiments. On such a view the primary effect would be the delay and prolongation of inhibition. During this period of delayed inhibition the post-ganglionic inhibitor neurone must be in a state of mild continuous activity. It is at least conceivable that impulses reaching it from the pre-ganglionic fibre under these conditions might interfere with the continuous excitation, the result being escape of the heart from inhibition while the stimulus lasts. There are, however, several objections to such a view. The effect of the first stimulation after administration of the paralytic drug is frequently a perceptible acceleration while the stimulus lasts, though this is naturally not so marked by contrast as the acceleration produced by subsequent stimulation during periods of delayed inhibition. Secondly, the acceleration is not a mere removal of the delayed inhibition: when the phenomenon has been well established by successive periods of stimulation, the acceleration frequently carries the rate above that which obtained subsequent to the administration of the drug, but prior to the first period of stimulation. Thirdly, a condition of not quite complete reversal is frequently met in which the first effect of the onset of each period of stimulation is to cause a further inhibition, lasting for a second or two, and followed by acceleration which then lasts till the stimulation is stopped. None of these features of the phenomenon can easily be reconciled with the hypothesis of inter¬ ference. The other, and on the. whole the more obvious explanation, is that the vagus contains, in addition to its normally predominant inhibitor fibres, others which produce acceleration of the heart-beat. The function of the paralyzing drug in this case would be discriminating, the accelerator action being revealed by depression of the inhibitor effect which normally masks it. If we accept the view that the vagus contains cardio-accelerator fibres, we could suppose these to be (a) pre-ganglionic autonomic fibres