# 1911 Encyclopædia Britannica/Aconite

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​ACONITE (Aconitum), a genus of plants belonging to the natural order Ranunculaceae, the buttercup family, commonly known as aconite, monkshood or wolfsbane, and embracing about 60 species, chiefly natives of the mountainous parts of the northern hemisphere. They are distinguished by having one of the five blue or yellow coloured sepals (the posterior one) in the form of a helmet; hence the English name monkshood. Two of the petals placed under the hood of the calyx are supported on long stalks, and have a hollow spur at their apex, containing honey. They are handsome plants, the tall stem being crowned by racemes of showy flowers. Aconitum Napellus, common monkshood, is a doubtful native of Britain, and is of therapeutic and toxicological importance. Its roots have occasionally been mistaken for horse-radish. The aconite has a short underground stem, from which dark-coloured tapering roots descend. The crown or upper portion of the root gives rise to new plants. When put to the lip, the juice of the aconite root produces a feeling of numbness and tingling. The horse-radish root, which belongs to the natural order Cruciferae, is much longer than that of the aconite, and it is not tapering; its colour is yellowish, and the top of the root has the remains of the leaves on it.
Many species of aconite are cultivated in gardens, some having blue and others yellow flowers. Aconitum lycoctonum, wolfsbane, is a yellow-flowered species common on the Alps of Switzerland. The roots of Aconitum ferox supply the famous Indian (Nepal) poison called bikh, bish or nabee. It contains considerable quantities of the alkaloid pseudaconitine, which is the most deadly poison known. Aconitum palmatum yields another of the celebrated bikh poisons. The root of Aconitum luridum, of the Himalayas, is said to be as virulent as that of A. ferox or A. Napellus. As garden plants the aconites are very ornamental, hardy perennials. They thrive well in any ordinary garden soil, and will grow beneath the shade of trees. They are easily propagated by divisions of the root or by seeds; great care should be taken not to leave pieces of the root about owing to its very poisonous character.
Chemistry.—The active principle of Aconitum Napellus is the alkaloid aconitine, first examined by P. L. Geiger and Hesse (Ann., 1834, 7, p. 267), Alder Wright and A. P. Luff obtained ​apoaconitine, aconine and benzoic acid by hydrolysis; while, in 1802, C. Ehrenberg and A. Purfürst (Journ. Prat. Chem., 1892, 45, p. 604) observed acetic acid as a hydrolytic product. This, and allied alkaloids, have formed the subject of many investigations by Wyndham Dunstan and his pupils in England, and by Martin Freund and Paul Beck in Berlin. But their constitution is not yet solved, there even being some divergence of opinion as to their empirical formulae. Aconitine (C$_{33}$H$_{45}$NO$_{13}$, according to Dunstan; C$_{34}$H$_{47}$NO$_{11}$, according to Freund) is a crystalline base, soluble in alcohol, but very sparingly in water; its alcoholic solution is dextrorotatory, but its salts are laevorotatory. When heated it loses water and forms pyraconitine. Hydrolysis gives acetic acid and benzaconine, the chief constituent of the alkaloids picraconitine and napelline; further hydrolysis gives aconine. Pseudaconitine, obtained from Aconitum ferox, gives on hydrolysis acetic acid and veratrylpseudaconine, the latter of which suffers further hydrolysis to veratric acid and pseudaconine. Japaconitine, obtained from the Japanese aconites, known locally as “kuza-uzu,” hydrolyses to japbenzaconine, which further breaks down to benzoic acid and japaconine. Other related alkaloids are lycaconitine and myoctonine which occur in wolfsbane, Aconitum lycoctonum. The usual test for solutions of aconitine consists in slight acidulation with acetic acid and addition of potassium permanganate, which causes the formation of a red crystalline precipitate. In 1905, Dunstan and his collaborators discovered two new aconite alkaloids, indaconitine in “mohri” (Aconitum chasmanthum, Stapf), and bikhaconitine in “bikh” (Aconitum spicatum); he also proposes to classify these alkaloids according to whether they yield benzoic or veratric acid on hydrolysis (Jour. Chem. Soc., 1905, 87, pp. 1620, 1650).
From the root of Aconitum Napellus are prepared a liniment and a tincture. The dose of the latter (Brit. Pharmacop.) is of importance as being exceptionally small, for it is not advisable to give more than at most five drops at a time. The official preparation is an ointment which contains one part of the alkaloid in fifty. It must be used with extreme care, and in small quantities, and it must not be used at all where cuts or cracks are present in the skin.
Pharmacology of Aconite and Aconitine.—Aconite first stimulates and later paralyses the nerves of pain, touch and temperature, if applied to the skin, broken or unbroken, or to a mucous membrane; the initial tingling therefore gives place to a long-continued anaesthetic action. Taken internally aconite acts very notably on the circulation, the respiration and the nervous system. The pulse is slowed, the number of beats per minute being actually reduced, under considerable doses, to forty, or even thirty, per minute. The blood-pressure synchronously falls, and the heart is arrested in diastole. Immediately before arrest the heart may beat much faster than normally, though with extreme irregularity, and in the lower animals the auricles may be observed occasionally to miss a beat, as in poisoning by veratrine and colchicum. The action of aconitine on the circulation is due to an initial stimulation of the cardio-inhibitory centre in the medulla oblongata (at the root of the vagus nerves), and later to a directly toxic influence on the nerve-ganglia and muscular fibres of the heart itself. The fall in blood-pressure is not due to any direct influence on the vessels. The respiration becomes slower owing to a paralytic action on the respiratory centre and, in warm-blooded animals, death is due to this action, the respiration being arrested before the action of the heart. Aconite further depresses the activity of all nerve-terminals, the sensory being affected before the motor. In small doses it therefore tends to relieve pain, if this be present. The activity of the spinal cord is similarly depressed. The pupil is at first contracted, and afterwards dilated. The cerebrum is totally unaffected by aconite, consciousness and the intelligence remaining normal to the last. The antipyretic action which considerable doses of aconite display is not specific, but is the result of its influence on the circulation and respiration and of its slight diaphoretic action.
Therapeutics.—The indications for its employment are limited, but definite. It is of undoubted value as a local anodyne in sciatica and neuralgia, especially in ordinary facial or trigeminal neuralgia. The best method of application is by rubbing in a small quantity of the aconitine ointment until numbness is felt, but the costliness of this preparation causes the use of the aconite liniment to be commonly resorted to. This should be painted on the affected part with a camel’s hair brush dipped in chloroform, which facilitates the absorption of the alkaloid. Aconite is indicated for internal administration whenever it is desirable to depress the action of the heart in the course of a fever. Formerly used in every fever, and even in the septic states that constantly followed surgical operations in the pre-Listerian epoch, aconite is now employed only in the earliest stage of the less serious fevers, such as acute tonsilitis, bronchitis and, notably, laryngitis. The extreme pain and rapid swelling of the vocal cords—with threatened obstruction to the respiration—that characterize acute laryngitis may often be relieved by the sedative action of this drug upon the circulation. In order to reduce the pulse to its normal rate in these cases, without at the same time lessening the power of the heart, the drug must be given in doses of about two minims of the tincture every half-hour and then every hour until the pulse falls to the normal rate. Thereafter the drug must be discontinued. It is probably never right to give aconite in doses much larger than that named. There is one condition of the heart itself in which aconite is sometimes useful. Whilst absolutely contra-indicated in all cases of valvular disease, it is of value in cases of cardiac hypertrophy with over-action. But the practitioner must be assured that neither valvular lesion nor degeneration of the myocardium is present.
Toxicology.—In a few minutes after the introduction of a poisonous dose of aconite, marked symptoms supervene. The initial signs of poisoning are referable to the alimentary canal. There is a sensation of burning, tingling and numbness in the mouth, and of burning in the abdomen. Death usually supervenes before a numbing effect on the intestine can be observed. After about an hour there is severe vomiting. Much motor weakness and cutaneous sensations similar to those above described soon follow. The pulse and respiration steadily fail, death occurring from asphyxia. As in strychnine poisoning, the patient is conscious and clear-minded to the last. The only post-mortem signs are those of asphyxia. The treatment is to empty the stomach by tube or by a non-depressant emetic. The physiological antidotes are atropine and digitalin or strophanthin, which should be injected subcutaneously in maximal doses. Alcohol, strychnine and warmth must also be employed.