The physiological action of choline and neurine / by F.W. Mott and W.D. Halliburton.

  • Frederick Walker Mott
Date:
1899
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Licence: Public Domain Mark

Credit: The physiological action of choline and neurine / by F.W. Mott and W.D. Halliburton. Source: Wellcome Collection.

Provider: This material has been provided by The Royal College of Surgeons of England. The original may be consulted at The Royal College of Surgeons of England.

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    a far-fetched idea to suppose that the continual pouring of small doses of choline into the cardiac tissue might in time produce cardiac weakness and even degeneratio]i. This possibility certainly still remains, but our study of the disease has now shown us that choline will not explain the fits, but that the fits will explain the degeneration in heart and other muscles. Such fatty degeneration probably never takes place unless fits have occurred before death ; and if similar fits occur in other diseases, as in the status epilepticus of epilepsy, there is the same fatty degeneration of the muscular tissues, even though no massive disintegration of nervous tissue has been present. Take again the point of enfeebled circulation; the pulse is often small and might be supposed to be associated with low tension. If this were the case, choline again would serve as the explanation. But on testing with the Hill-Barnard sphygmo- meter the arterial tension in these patients, low tension was not the rule but the exception.* Evidently choline is not the cause of this ; choline alone would produce low tension from dilatation of peripheral vessels. Our experiments with atropine are most instructive from this standpoint; we have seen (p. 260) that the previous sub- cutaneous injection of a minute dose of atropine, mixed with morphine, will modify the result of the injection of choline very considerably, for, under these circumstances, choline now produces a rise instead of a fall of arterial blood-pressure. We do not, of course, mean to suggest that atropine, or even a similar alkaloid, is present in these patients, but these experiments do suggest that with a plurality of causes we undoubtedly obtain an intermixture or even a reversal of effects. We have been able to work out fairly thoroughly the physiological action of choline and neurine, but, so far as we can see at present, the result is rather of academic than of direct practical value in the elucidation of pathological problems. No doubt, with fresh light which future work may throw on our own, it may be possible to see the modus operandi of these pathological processes more clearly, and our three years’ work will not have been thrown away if it forms some sort of guidance to others, or to ourselves, in unravelling the plurality of causes to which we have just alluded, and which we must assume is present in General Paralysis as in so many other obscure diseases. The expenses involved in this research have been defrayed from grants made by the Government Grant Committee of the Royal Society, and by the British Association. * See Supplementary Note C at the end of this Paper. VOL. CXCI. B. 2 M