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Abies Spectabilis (D. Don) G. Don (Syn. A. Webbiana Lindl.) Family: Coniferae
Published in L.D. Kapoor, Handbook of Ayurvedic Medicinal Plants, 2017
Pharmacological action — Mild stomachic, bitter tonic, diuretic, and antilithic. Hayatin and its various derivatives were found to possess neuromuscular blocking action. Low doses of hayatin methiodide had little effect on blood pressure, but higher doses caused a fall in intact spinal dogs, rabbits, and cats. The drug had little action on heart, isolated or in situ269 Hayatin methiodide and methochloride possessed almost an equal degree of curariform activity as compared to d-tubocurarine chloride.270 Hayatin methochloride possessed similar muscle-relaxant properties to d-tubocurarine chloride in cats, dogs, mice, and rabbits.271
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Published in Anton Sebastian, A Dictionary of the History of Medicine, 2018
Curare A nonspecific term for a group of South American arrow poisons called woorara and obtained from the roots of the vine, Strychnos toxifera. The first mention was made by an Italian scholar and historian, Peter Martyr Angherius (1455–1526) in 1516. The effects of the poison known as woorali were described by Sir Walter Raleigh (1552–1618) on his voyage to British Guiana in 1595. Charles Marie de la Condamine (1701–1704), a French scientist and explorer, brought it from the Amazon to Europe around 1743. Alexander von Humboldt (1769–1859) was one of the first to describe the poison in detail in 1799. In 1811 Sir Benjamin Brodie (1783–1862), in his experiments on animals, used it to paralyze and kept them alive by maintaining their respiration with bellows. Woorali was described as a poison ‘that destroys life so gently, that the victim appears to be in no pain whatever’by Charles Waterton (1782–1865) in Wanderings in South America, published in 1825. Its paralyzing effect on the myoneural junction in frogs was demonstrated by Claude Bernard (1813–1878) in 1840. It was first used in medical practice to relax the muscles in rabies in 1838, in tetanus in 1858, and in epilepsy in 1860. It was used during surgery by German physician, Laewen of Zwickau, to produce muscle relaxation in 1912. However, the significance of Laewen’s discovery went unnoticed for two decades. In 1935, Harold King, a Welsh chemist obtained a pure form, D-tubocurarine, and Archibald R. McIntyre and A.E. Bennett obtained the same substance from the bark of Chondodendron tomentosum from Ecuador in 1939. A standardized form, called Intocostrin, was produced in the same year. Frederick Prescott demonstrated its clinical use through self-experimentation. Scott M. Smith, a surgeon from Utah, also conducted experiments on himself in 1943, and the drug, as tubocurarine chloride, subsequently became established as a muscle relaxant in anesthesia. See arrow poisons.
In vitro models of neuromuscular junctions and their potential for novel drug discovery and development
Published in Expert Opinion on Drug Discovery, 2020
Olaia F Vila, Yihuai Qu, Gordana Vunjak-Novakovic
Tubocurarine chloride pentahydrate, a toxic alkaloid and muscle relaxant that was used with anesthetics in the mids-1900s, is one of the postsynaptic blockers most commonly used in NMJ studies. Treatment with tubocurarine has been shown to dim or stop both spontaneous [38] and glutamate-induced [35] contractions in motoneuron-muscle co-cultures, as well as in mouse microfluidics [54] and human [57] tissue-engineered systems. Smith et al. also showed that tubocurarine was able to block the glutamate-induced contractions in their cantilever system [56]. In addition to these qualitative studies, a dose-response curve performed in a compartmentalized microfluidic system demonstrated an IC50 in agreement with reported results for human AChRs [72,73].