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Panax quinquefolium (American Ginseng) and Physostigma venenosum (Calabar Bean)
Published in Azamal Husen, Herbs, Shrubs, and Trees of Potential Medicinal Benefits, 2022
Sushweta Mahalanobish, Noyel Ghosh, Parames C. Sil
CB, Physostigma venenosum, also known as “ordeal bean”, is a leguminous, woody climbing plant in nature and is mainly found in the tropical forests of Western Africa. (Proudfoot, 2006). Etymologically, Physostigma has been named due to the presence of a beak-like appendage at the end of the stigma within the center of its flower. The plant is an herbaceous, perennial having a woody stem as its base. This is a scarlet runner bean with a height of 50 feet and a diameter of two inches. The flowers are large, heavily veined, pale pink or purplish in color, generally an inch long with axillary peduncles, and grouped in pendulous, fascicled racemes. The seed pods containing two or three seeds are 6–7 inches in length. The beans are similar to horse bean but less flattened and chocolate-brown in appearance (Swain, 1972).
Plant Alkaloids and Their Derivatives Relevant to Alzheimer’s Disease
Published in Atanu Bhattacharjee, Akula Ramakrishna, Magisetty Obulesu, Phytomedicine and Alzheimer’s Disease, 2020
Atanu Bhattacharjee, Akula Ramakrishna
Physostigmine [Figure 17.2(i)] is a reversible AChE inhibitor, originally isolated from the seed of Physostigma venenosum (Family: Fabaceae). It enhances short-term memory in dementia patients and is used to treat mild to moderate AD (Urbain et al., 2004).
Cholinergic Agonists
Published in Sahab Uddin, Rashid Mamunur, Advances in Neuropharmacology, 2020
Rupali Patil, Aman Upaganlawar
Physostigmine/eserine, a tertiary amine, is an alkaloid isolated by Jobst and Hesse in 1864. It was obtained from Calabar (ordeal) bean that was obtained from the dried, ripe seeds of a perennial plant of Physostigma venenosum. Calabar beans were used in witchcraft trials, in which guilt was judged by death from the poison, innocence by survival after ingestion of a bean. For the first time in 1877, physostigmine was used therapeutically that Laqueur used for the treatment of glaucoma during his clinical practice (Karczmar, 1970; Holmstedt, 2000; Brunton, 2011).
Pyrethroid based pesticides – chemical and biological aspects
Published in Critical Reviews in Toxicology, 2021
Anandha Rao Ravula, Suresh Yenugu
CAs are derived from carbamic acid and the first one among this class, carbaryl, was introduced in 1956 as a lawn and garden insecticide. Its broad-spectrum insect control activity and low toxicity to mammals allowed it to be a preferred choice. CAs are less persistent in the environment unlike OPs and OCs and are rapidly detoxified in animal tissues. The mode of action of CAs is similar to that of OPs as both are inhibitors of acetylcholinesterase (AChE). While CAs inhibit AChE activity by phosphorylation resulting in the formation of a reversible complex, OPs form an irreversible complex (Darvesh et al. 2008). Since CAs are considered to be safer than OPs, as they exhibit reversible action on AChE and do not cause severe poisoning in cholinergic pathway (Silva et al. 2013), they are proposed as therapeutic drugs (physostigmine derived from Physostigma venenosum) for neuromuscular disorders such as myasthenia gravis.
Physostigmine is superior to non-antidote therapy in the management of antimuscarinic delirium: a prospective study from a regional poison center
Published in Clinical Toxicology, 2019
Sean P. Boley, Travis D. Olives, Stacey A. Bangh, Samuel Fahrner, Jon B. Cole
Physostigmine has been known to effectively reverse central antimuscarinic toxicity for over 150 years [4]. The earliest published reported use of physostigmine for antidotal purposes was by Kleinwachter in 1864 [5] to reverse the mydriasis caused by the ingestion of atropine [6]. Almost 100 years later, Forrer and Miller [7] reported the use of physostigmine to reverse antimuscarinic delirium in humans in the setting of atropine-induced comas for the treatment of psychosis. Derived from the Calabar bean (Physostigma venenosum), the drug reached its peak use during the 1960s and 1970s [8], when it was considered not only to be a part of the “coma cocktail” for the treatment of undifferentiated delirium [9], but was also used to treat the cardiovascular and central nervous system effects of tricyclic antidepressants (TCAs) [10–12]. The use of physostigmine declined [5] following a two patient case series published in 1980 by Pentel and Peterson [13] that reported two episodes of asystole temporally associated with physostigmine administration. Despite this, several researchers have continued to investigate the safety and efficacy of the antidote [8,14–17]. Multiple observational studies have demonstrated the safety of physostigmine in a variety of contexts [15–18], but few have compared physostigmine use to non-antidote therapy in a prospective fashion, and none have done so via telephone recommendations from a regional poison center (PC). Therefore, we prospectively compared the use of physostigmine to non-antidotal therapy in the treatment of antimuscarinic delirium. Furthermore, we set out to characterize the impact of physostigmine use on resource utilization (intubation and restraint use) and adverse event rates (vomiting, bradycardia, seizures).