Scientific Name(s): Aconitum napellus L., Aconitum carmichaelii Debeaux, and Aconitum kusnezoffii Rchb. Family: Ranunculaceae.
Common Name(s): Aconite , aconite tuber , monkshood , friar's cap , helmet flower , soldier's cap , wolfsbane , devil's helmet , blue rocket , leopard's bane , chuanwu , caowu , wutou , futzu , bushi , ,
Aconite extracts have been used homeopathically in Europe and Asia (orally and externally), but rarely in the United States. Use is not recommended because of its toxicity.
Extreme caution is required. Fresh aconite is extremely toxic, and safe dosage is dependent on processing. Many species are used medicinally in China only after processing. Traditional Western texts recommended 60 mg of the root per dose.
Contraindications have not been identified.
Documented adverse effects. In addition to oral administration, external application is reported to cause toxic symptoms. Avoid use.
None well documented.
Aconitine is highly toxic. As little as 2 mg of pure aconite or 1 g of plant may cause death from paralysis of the respiratory center or cardiac muscle. Clinically important toxicity may develop following percutaneous absorption; even slight contact with the flowers can cause fingers to become numb.
Aconitine is an alkaloid derived from various species of Aconitum . At least 350 species exist throughout the world; about 170 species exist in China, and more than 100 species are found throughout the temperate zones of the United States and Canada. The plants are also found throughout many parts of Asia, Africa, and Europe. A. napellus is the most common species in Europe, and has been naturalized in the eastern United States; A. carmichaelii and A. kusnezoffii are the most common species used in traditional Chinese medicine. Aconitum species are erect perennial plants growing to a height of 0.6 to 1.5 m (2 to 6 feet). In general, they resemble delphiniums. The characteristic helmet-shaped blue or purple flowers grow in a raceme at the top of the stalk in summer or fall. Occasionally, the flowers may be white, pink, peach, or yellow. The seed pods contain numerous tiny seeds.
Various species of Aconitum have been used for centuries both as poisons and medicines. Some are still being used in traditional medicines of India, China, and Japan. The root is the most toxic, although all parts of the plant are considered to be toxic. The toxicity of the extracts follow the same order as the alkaloid content: roots, flowers, leaves, and stems.
Extracts of the Aconitum species have been used orally in traditional medicine to reduce fever associated with colds, pneumonia, laryngitis, croup, and asthma; and for their analgesic, anti-inflammatory, hypotensive, diuretic, diaphoretic (cause sweating), cardiac depressant (slow heart rate), and sedative properties. , In traditional Asian medicine, root extracts are typically mixed with other ingredients, such as licorice or ginger. Extracts also have been used as arrow poisons.
Historically, aconite was most commonly used in Western cultures as a tincture. It was applied topically as a counter irritant liniment for neuralgia, rheumatism, and sciatica.
In homeopathy, aconite is used to treat fear, anxiety, and restlessness; acute sudden fever; symptoms from exposure to dry, cold weather or very hot weather; tingling, coldness, and numbness; influenza or colds with congestion; and heavy, pulsating headaches.
Alkaloids account for up to 1.5% of the dry weight of Aconitum plant species. A wide variety of alkaloids have been isolated from the various species of aconite, including the major active alkaloid aconitine, as well as mesaconitine, hypaconitine, jesaconitine, napelline, sinomontanitines, lappaconitine, ranaconitine, and others. , , , , , Other alkaloids may be produced by processing (eg, pyro-type aconitine alkaloids by heat or benzylaconines or aconines by hydrolysis). Aconitine and its congeners are considerably more toxic than aconine and related alkaloids.
Uses and Pharmacology
Because aconite is highly toxic, its use is not recommended. Raw aconite products are extremely toxic; their alkaloids have a narrow therapeutic index and the alkaloid type and amount vary with species, place of harvest, and adequacy of processing. Processing may reduce alkaloid content and/or alter alkaloid composition, thus reducing potency; however, poisoning may still occur after the consumption of processed aconite root.
The following pharmacological effects of Aconitum alkaloid have been described: analgesic, anti-inflammatory, and anti-rheumatic activity , ; positive inotropic effects ; and regulation of neurological disorders. , However, only limited studies are available, and most were performed in China and Japan.Animal data
In animal models, aconitine and related compounds have been shown to possess anti-inflammatory and analgesic properties. , , Studies using mechanical and thermal stimuli to cause pain in mice have shown that, at sub-analgesic doses, processed Aconitum root administered orally, both partially and dose-dependently inhibited the development of morphine tolerance in morphine-naive mice and reversed already developed morphine tolerance in morphine-tolerant mice when compared with placebo. , , ,Human data
Results of a study using Japanese kampo preparations suggest that Aconiti tuber may increase nitric oxide production in humans, a possible mechanism for its purported effect on improving a peripheral feeling of coldness. Eleven and 13 patients, respectively, received kampo formulas including and excluding Aconiti tuber. The nitrite and nitrate levels were increased at 4 weeks in those taking Aconiti tuber formulas.Clinical data
Research reveals no clinical data regarding the use of aconite for medical purposes.
Guanfu base A, a new alkaloid isolated from the root of A. coreanum Rapaics, has been found to be an effective antiarrhythmic agent in preclinical and clinical studies and is now undergoing phase 3 clinical trials in China.
Shenfu injection, a traditional Chinese therapy that contains red ginseng and aconite root, has provided a protective effect against ischemia and reperfusion injury during mitral valve replacement with cardiopulmonary bypass, and has also stimulated the immune system and reduce blood viscosity, improving postoperative recovery after abdominal surgery. However, the effect of the aconite component has not been determined.
Extreme caution is required. Fresh aconite is extremely toxic, and safe dosage is dependent on processing. Many species are used medicinally in China after processing. Traditional Western texts recommended 60 mg of the root per dose. Pure aconite 2 mg or aconite plant 1 g may cause death.
Documented adverse effects. Even external application is reported to cause toxic symptoms. Avoid use.
None well documented.
Because aconite is not considered safe for human use, all effects are considered toxic.
Aconite is a fast-acting toxin. The active principles are aconitine and related alkaloids. Pure aconite 2 mg or aconite plant 1 g may cause death.
Toxicity and death have resulted when the plant has been consumed accidentally, possibly mistaken for wild parsley, horseradish, or other herbs growing in the wild. , Very few cases of aconite poisoning have been reported in North America. Most reports have been related to the use of traditional Chinese remedies. A retrospective search of the Taiwan National Poison Center database between 1990 and 1999 revealed 17 cases of aconitine poisoning. Thirteen patients ingested aconite root for treatment of rheumatism or wounds. Two patients had volunteered to test the effects of aconite root in a drug study. Only 2 patients had accidentally ingested the root. The Toxicology Reference Laboratory in Hong Kong confirmed 10 cases of aconite poisoning between March 2004 and May 2006. In 4 cases, the aconite herb was not listed in written prescriptions.
Most incidents of aconite toxicity result from the wide variability in strength of home preparations in Asian countries. However, more lethal poisonings are being reported in Western countries where the use of herbal remedies is increasing. , A homicide attempt and a suicide with the plant have been reported.
Aconitine's toxicity is characterized by a burning or tingling sensation of the lips, tongue, mouth, and throat almost immediately following ingestion. Numbness of the throat and difficulty with speech may ensue. Salivation, nausea, vomiting, dizziness, and diarrhea may occur, as well as visual blurring or yellow-green color vision distortion, weakness, and incoordination. Paraesthesia may spread over the entire body. Toxicity mainly affects CNS, heart, and muscle tissues, primarily resulting in cardiovascular complications. , , , , Cardiac arrhythmias with unusual electrical characteristics have been observed following aconite poisoning. , Putrescine, a compound used experimentally as a molecular probe, has been shown to attenuate aconitine-induced arrhythmias. Death from aconitine may follow, secondary to cardiac arrhythmia, which can occur unpredictably within minutes or days. Several case reports describe poisonings with aconite or its constituents, resulting in ventricular tachycardia, other arrhythmias, and death. , , , , ,
A single dose of aconitine 0.6 mg/kg administered intraperitoneally to rabbits caused histopathologic damage to the myelin sheath of the visual pathway, spinal cord, and peripheral nerves. Similarly, aconitine has demonstrated arrhythmogenic and cardiotoxic effects on myocardium in anesthetized cats. Some experiments have used aconitine to artificially induce arrhythmias in laboratory animals to study the antiarrhythmic effects of other drugs. ,
A review has summarized the toxicological mechanisms of Aconitum alkaloids, which include the following: (1) binding to voltage-dependent sodium channels inducing a hyperpolarized state, resulting in permanent activation of the channel; (2) modulation of neurotransmitter release and receptors, particularly norepinephrine and acetylcholine; (3) promotion of lipid peroxidation of the cardiac system, possibly causing cardiac arrhythmias; and (4) induction of cellular apoptosis in the heart, liver, and other organs. Most of the cardiotoxic and neurotoxic effects can be explained by these mechanisms, including their effect on calcium imbalance.
General supportive measures, including fluids for dehydration, intravenous pressor agents (eg, dobutamine, dopamine) for hypotension, and resuscitative measures when indicated, form the basis of aconite toxicity management. , Gastric lavage or induction of emesis following the injection of atropine has been recommended. Control of cardiac dysrhythmias has been attempted with various antiarrhythmic agents (eg, lidocaine, amiodarone, flecainide, procainamide, mexiletine) ; however, no single antiarrhythmic drug has been uniformly effective. , Amiodarone and flecainide have been reasonable first-line choices. , , Several cases of successful treatment using percutaneous cardiopulmonary support and bypass in the first 24 hours have been reported. , , Charcoal hemoperfusion has also been used in patients with ventricular arrhythmias unresponsive to antiarrhythmic agents and supportive care, and may have played a critical role in patient survival. , Recovery time is dependent on amount of intoxication; mildly intoxicated patients may take 1 to 2 days to recover, whereas patients with cardiovascular complications may take 7 to 9 days to recover.
Evidence suggests that aconite may lose potency after undergoing certain manufacturing procedures; therefore, processed aconite may not have a toxicity profile similar to that of crude plant material.
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