A manual of pharmacology / by Walter E. Dixon.

  • Dixon, Walter E. (Walter Ernest), 1871-1931.
Date:
1929
Catalogue details

Licence: In copyright

Credit: A manual of pharmacology / by Walter E. Dixon. Source: Wellcome Collection.

    504/534 page 468
    best example is, perhaps, that of the nitrites and barium on the vessels. The nitrites depress muscle-fibre and so dilate the vessels, barium excites the muscle and so tends to constrict the vessels; but whether the two drugs act on the same constituent in the muscle-fibre it is impossible to say. On cardiac muscle such drugs as chloroform, chloral, and potassium diminish the force of con- traction and increase the relaxation, whilst barium and veratrine, on the contrary, increase the force of contraction and diminish relaxation. Hence, these drugs are antagonistic to one another. On such an organ as the heart many drugs produce antagonistic effects without acting on the same structure: aconitine and caffeine, by stimulating the excito-motor area, quicken the heart, and this effect is in a limited degree antagonised by pilocarpine, which excites the vagal endings. Or the effect of a big dose of pilo- carpine, which tends to slow the heart through the vagus, is annulled by an injection of adrenalin, which quickens the heart through the accelerator nerve. The antagonistic action of drugs on nerve-endings is best illus- trated by that of atropine and pilocarpine. Pilocarpine produces slowing of the heart, a copious flow of saliva and sweat, constriction of the pupil, and increased movements of plain muscle generally. These effects are antagonised in each case by atropine, which paralyses some portion of the nerve-endings, thereby interfering with the action of the former drug. Physostigmine, which has many effects resembling pilocarpine, is also antagonised by the atropine group of drugs. Again, digitalis excites the nerve-endings in the vagus, and so tends to slow the heart and to increase the peristaltic movements of the alimentary canal. These effects are also antagonised by atropine. And, lastly, adrenalin excites the nerve-endings of the sympathetic; apocodeine paralyses these same nerve-endings, and so abolishes the adrenalin effect. Ergotoxin paralyses those structures which adrenalin stimulates. So that where the nerve-supply from the sympathetic system is purely inhibitory ergotoxin is without action either on the adrenalin effect or on sympathetic nerve stimulation (stomach, intestines, gall-bladder). If the sympathetic supply is purely motor the action of adrenalin or nerve stimulation is annulled (heart, dilator iridis, retractor penis, pilo-motor muscles, and ileo-colic sphincter). And if the sympathetic supply is mixed, ergotoxin removes the motor effects and leaves the inhibitory (the arteries of carnivora, spleen, uterus, etc.). Ergotoxin clearly, then, has a very specialised selec- tive action on the motor elements of that structure, which is excited by adrenalin and by impulses in fibres of the true sympathetic system, the inhibitor elements being unaffected. The motor effects of pilocarpine on the pregnant uterus are antagonised by ergotoxin injected previously, whilst the inhibitory action is unimpaired, and in this pilocarpine resembles adrenalin; but the pilocarpine effect is completely antagonised by atropine, whilst the adrenalin action
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