• Source: Alcuronium chloride

Alcuronium chloride (formerly marketed as Alloferin) is a neuromuscular blocking (NMB) agent, alternatively referred to as a skeletal muscle relaxant. It is a semi-synthetic substance prepared from C-toxiferine I, a bis-quaternary alkaloid obtained from Strychnos toxifera. C-toxiferine I itself has been tested for its pharmacological action and noted to be a very long acting neuromuscular blocking agent For a formal definition of the durations of actions associated with NMB agents, see page for gantacurium. The replacement of both the N-methyl groups with N-allyl moieties yielded N,N-diallyl-bis-nortoxiferine, now recognized as alcuronium.
Inclusion of the allylic functions presented an enhanced potential area of biotransformation, and thus alcuronium is observed to have a much shorter duration of neuromuscular blocking action than its parent C-toxiferine I. It also has a more rapid onset of action, and is ~1.5 times as potent as tubocurarine. The pharmacological action of alcuronium is readily reversed by neostigmine, and it produces little histamine release. The major disadvantage of alcuronium is that it elicits a vagolytic effect produced by a selective atropine-like blockade of cardiac muscarinic receptors.




Effects


Cardiovascular system: histamine release and blockage of the sympathetic ganglia including adrenal medulla could cause hypotension
Respiratory system: apnea due to phrenic blockage but bronchoconstriction can occur from the histamine release
Central nervous system: no effect on intraocular pressure
Autonomic ganglion blockade can cause a decrease in gut motility




Special points


Duration of action prolonged in states of low potassium, calcium and protein, also in states of high magnesium and acidosis.
Pharmaceutically incompatible with thiopentone
Infusion can cause fixed dilated pupils




See also


The International Pharmacopoeia




References






Further reading


Zahn K, Eckstein N, Tränkle C, Sadée W, Mohr K (2002). "Allosteric modulation of muscarinic receptor signaling: alcuronium-induced conversion of pilocarpine from an agonist into an antagonist". J Pharmacol Exp Ther. 301 (2): 720–8. doi:10.1124/jpet.301.2.720. PMID 11961078. S2CID 534003.
Maass A, Mohr K (1996). "Opposite effects of alcuronium on agonist and on antagonist binding to muscarinic receptors". Eur J Pharmacol. 305 (1–3): 231–4. doi:10.1016/0014-2999(96)00240-3. PMID 8813558.
Jakubík J, Tucek S (1994). "Protection by alcuronium of muscarinic receptors against chemical inactivation and location of the allosteric binding site for alcuronium". J Neurochem. 63 (5): 1932–40. doi:10.1046/j.1471-4159.1994.63051932.x. PMID 7931349. S2CID 23053191.
Proska J, Tucek S (1994). "Mechanisms of steric and cooperative actions of alcuronium on cardiac muscarinic acetylcholine receptors". Mol Pharmacol. 45 (4): 709–17. PMID 8183250.

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