Neuromuscular Blocking Drugs
Pancuronium, Vecuronium, Rocuronium, Tubocurarine
Atracurium, Mivacurium, Cisatracurium,
It is actually two ACh molecules back-to-back.
Broken down by Plasma Cholinesterase.
Sux enters the receptor site and causes depolarisation
Atracurium = Hofmann elimination and ester hydrolysis (non-specific)
Mivacurium = Short-acting, rapidly hydrolysed by plasma cholinesterase.
Cisatracurium = Isomer.15% of the mixture of atracurium. 4x more potent.
Undergoes organ-independent degradation, tend to release histamine.
Rocuronium is 6-8 times less potent than vecuronium.
Rocuronium is more lipophilic than vecuronium
Most of the Roc is taken up by the liver and eliminated via the bile.
Vecuronium is provided as a powder, releases no histamine.
Most do not have any CVS effects
Rocuronium at high doses = vagolytic.
These drugs block ACh from binding to the receptor site so end plate potentials don't develop
The Hofmann rearrangement (degradation) is the organic reaction of a primary amide to a primary amine with one fewer carbon atoms.
A metabolite of Hofmann degradation (laudanosine) is a tertiary amine that has epileptogenic properties in high concentration, although this complication has not been reported in humans during general anaesthesia.
They consist of two quaternary ammonium groups joined by a thin chain of methyl groups.
They are more liable to breakdown in the plasma than the aminosteroid compounds. They lack any vagolytic effect but are more likely to release histamine. The methyl chain contains one or more chiral atoms, which leads to the existence of several stereoisomers of these drugs.
Aminosteroid compounds contain an androstane skeleton to which ACh-like moieties are introduced at the A ring and D ring.
They tend not to cause histamine release.
Most depend on organ function for their excretion.
Some undergo deacetylation in the liver, and the deacetylated metabolites may possess neuromuscular blocking properties.
Dr. David Lyness