Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
N (what isYN ?)
Infobox references
Chemical compound
Laudanosine or N-methyltetrahydropapaverine is a recognized metabolite[1] of atracurium and cisatracurium. Laudanosine decreases the seizure threshold, and thus it can induce seizures if present at sufficient threshold concentrations; however such concentrations are unlikely to be produced consequent to chemodegradable metabolism of clinically administered doses of cisatracurium or atracurium.
Capsule of Papaver somniferum showing latex (opium) exuding from incision. Laudanosine occurs naturally in small amounts (0.1%) in opium.
Laudanosine also occurs naturally in minute amounts (0.1%) in opium, from which it was first isolated in 1871.[2] Partial dehydrogenation of laudanosine will lead to papaverine, the alkaloid found in the opium poppy plant (Papaver somniferum).
Laudanosine is a alkaloid. It has been shown to interact with GABA receptors, glycine receptors, opioid receptors, and nicotinic acetylcholine receptors,[1][3][4] but not benzodiazepine or muscarinic receptors, which are also involved in epilepsy and other types of seizures.[5]
^Burger A (2005) [1954]. "The Benzylisoquinoline Alkaloids". In Manske RH, Holmes HL (eds.). The Alkaloids: Chemistry and Physiology. 4. New York: Academic Press. p. 48. ISBN0-12-469504-3. Retrieved September 18, 2008 through Google Book Search.
^Katz Y, Weizman A, Pick CG, Pasternak GW, Liu L, Fonia O, Gavish M (May 1994). "Interactions between laudanosine, GABA, and opioid subtype receptors: implication for laudanosine seizure activity". Brain Res. 646 (2): 235–241. doi:10.1016/0006-8993(94)90084-1. PMID8069669. S2CID35031924.
^Katz Y, Gavish M (Jan 1989). "Laudanosine does not displace receptor-specific ligands from the benzodiazepinergic or muscarinic receptors". Anesthesiology. 70 (1): 109–111. doi:10.1097/00000542-198901000-00020. PMID2536252.