Aconite

ACONITE, Aconitum Napellus L., monkshood, a perennial herbaceous plant of the buttercup family (Ranunculaceae), distributed in the mountains of central and southern Europe, the Caucasus, Turkestan, Siberia, the Himalayas, and North America; in gardens it is cultivated as an ornamental plant. The stem of A. reaches 1–1.5 m in height; leaves, 3–7-lobed, with narrowly wedge-shaped lobes, sit on long petioles; blue-purple flowers appear in a long raceme at the top of the stem in the second half of summer. The root consists of two black-brown tuberous tubers, from which one is the maternal—last year's, shriveled—and gives rise to the stem, while the other is the daughter—young, fleshy, bearing the apical bud for the stem of the coming year. In medicine, the tubers of the plant are used, dug up in autumn or during the flowering of aconite, and the herb (leaves and flower racemes), from which extracts and alcoholic tinctures are prepared. According to VII, tinctura Aconiti is prepared from daughter tubers collected in autumn from wild aconite. Aconite is a very poisonous plant, containing alkaloids in all its parts, and especially in the daughter tubers: aconitine, benzoyl-aconine (picro-aconitine, napelline), pseudo-aconitine (neopalline), which in chemical terms are ether-like compounds of the aconine base with acetic, benzoic, and veratric acids. Such compounds also include the alkaloids: japaconitine, indaconitine, and bikhaconitine, found in other species of aconite (A. japonicum, A. ehasmanthum, A. spicatum). Amorphous bitter aconine (C₂₅ H_u N0₉) is obtained, as such, from A. and represents the final product in the hydrolysis of crystalline aconitine or benzoyl-aconine. From crystalline A., as a product of decomposition, crystalline alkaloid pyraconitine (Csi H₄₁NO_M) is also obtained. The action of aconitines is very diverse and far from fully studied. Aconitine, Cs4 H„ NOu, is best studied in this regard, considered as acetyl-benzoyl-aconine. Aconitine is a colorless crystalline powder of a sharp burning but not bitter taste, melting at 197–198°, difficultly soluble in water, easily soluble in alcohol, ether, chloroform; the aqueous solution has an alkaline reaction and is optically dextrorotatory; aconitine with nitric, hydrochloric, hydrobromic, and other acids forms crystalline salts, well soluble in water; the solution of nitric acid aconitine deviates the plane of polarization to the left. The action of A. on the organism is characteristic, initially expressed as excitation of the endings of all motor, sensory, and secretory nerves, as well as the vagus nerves, and then paralysis of them: fibrillary contractions of muscles, twitchings, a sensation of general heat, crawling ants, chills, aches, burning pains throughout the body, especially in the area of the branching of the trigeminal nerve (skin of the head and face) and in the intestines; increased secretion of saliva, sweat, urine; slowing of heartbeats, which is preceded by a brief acceleration due to the primary irritation of aconitine of the motor nodes of the heart, soon replaced by paralysis of these ganglia. After that, very characteristic peristaltic contractions of the heart (Hartung) appear together with weakening of the pulse and falling blood pressure; slowing and difficulty of breathing, which occur after a brief excitement of breathing; expiratory dyspnea with stops of respiratory movements in the exhalation phase, and finally complete cessation of breathing due to paralysis of the respiratory center; violent peristalsis of the intestines, often vomiting; convulsions, constriction of the pupils, in the further course—diminution of vision, hearing, paresthesias, paralysis of movements, clouding of consciousness—signs of the deep influence of A. on the central nervous system. Death occurs from cessation of breathing. Therapeutically, preparations of A. were applied for local anesthesia and as an antineuralgic agent, especially in trigeminal neuralgias, but due to the great toxicity of A., all its preparations have gone out of use. The toxic significance of A. is very great, since poisonings by it are frequent. The lethal dose of chemically pure aconitine is considered for humans to be a dose of 4 mg, and for animals 0.02–0.05 mg per kilogram of animal weight. The aconitine found for sale may be of different quality and strength of action; in trade, aconitine is distinguished by varieties—German, French, and English. Assistance in poisoning by A. or its preparations: artificial respiration; subcutaneous sulfuric atropine, caffeine, adrenaline; wash out the stomach and intestines; give a laxative internally. In legal cases, opening and establishing the chemical presence of aconitine by chemical reactions is not successful; therefore, the best method is a physiological experiment on a dissected frog heart (Filhner).