The gastrointestinal features include nausea, vomiting, abdominal pain, and diarrhea. The cardiovascular features include hypotension, chest pain, palpitations, bradycardia, sinus tachycardia, ventricular ectopics, ventricular tachycardia, and ventricular fibrillation. The neurological features can be sensory (paresthesia and numbness of face, perioral area, and the four limbs), motor (muscle weakness in the four limbs), or both. Patients present predominantly with a combination of neurological, cardiovascular, and gastrointestinal features. Aconitine, mesaconitine, and hypaconitine can induce strong contractions of the ileum through acetylcholine release from the postganglionic cholinergic nerves. Through its action on voltage-sensitive sodium channels in the axons, aconitine blocks neuromuscular transmission by decreasing the evoked quantal release of acetylcholine. It has hypotensive and bradycardic actions due to activation of the ventromedial nucleus of the hypothalamus. Aconitine has a positive inotropic effect by prolonging sodium influx during the action potential.

The arrhythmogenic properties of aconitine are in part due to its cholinolytic (anticholinergic) effects mediated by the vagus nerve. The electrophysiological mechanism of arrhythmia induction is triggered activity due to delayed after-depolarization and early after-depolarization. Aconitine and mesaconitine bind with high affinity to the open state of the voltage-sensitive sodium channels at site 2, thereby causing a persistent activation of the sodium channels, which become refractory to excitation. The cardiotoxicity and neurotoxicity of aconitine and related alkaloids are due to their actions on the voltage-sensitive sodium channels of the cell membranes of excitable tissues, including the myocardium, nerves, and muscles. Key articles with information on the use of aconite roots in traditional medicine, active (toxic) ingredients, mechanisms of toxicity, toxicokinetics of Aconitum alkaloids, and clinical features and management of aconite poisoning were reviewed. However, the use of a larger than recommended dose and inadequate processing increases the risk of poisoning.Ī Medline search (1963-February 2009) was conducted. Soaking and boiling during processing or decoction preparation will hydrolyze aconite alkaloids into less toxic and non-toxic derivatives. In traditional Chinese medicine, aconite roots are used only after processing to reduce the toxic alkaloid content. Severe aconite poisoning can occur after accidental ingestion of the wild plant or consumption of an herbal decoction made from aconite roots. The wild plant (especially the roots and root tubers) is extremely toxic. Genitival interfix used to link elements in some compounds, equivalent to the possessive clitic -'s.Īny of several poisonous perennial herbs of the genus Aconitum.Aconitine and related alkaloids found in the Aconitum species are highly toxic cardiotoxins and neurotoxins.

A white worm, or maggot, which infests granaries.

A man who makes amorous advances on many women. (figurative) Any very ravenous, rapacious, or destructive person or thing especially, want starvation. (transitive) To devour to gobble to eat (something) voraciously. (transitive) To kill, especially by poison to be the poison of. (chiefly, Scotland) bone (transitive) To be the bane of. A cause of misery or death an affliction or curse. (dated) Poison, especially any of several poisonous plants. Detailed word origin of wolfsbane Dictionary entry

Wolfsbane meaning