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Alcuronium
See also Neuromuscular blocking drugs, non-depolarizing
General information
Alcuronium is a synthetic derivative of toxiferine, an alkaloid of calabash curare, and is a non-depolarizing relaxant with properties and adverse effects similar to those of D-tubocurarine. It is about twice as potent as D-tubocurarine, 0.15–0.25 mg/kg usually being adequate for abdominal relaxation, and has a similar onset time and a slightly shorter duration of action. It is bound to albumin (40%), and requirements for alcuronium are less if the plasma albumin levels are low, as may occur in hepatic disease.
Like d -tubocurarine, alcuronium does not undergo biotransformation. Excretion occurs mainly in the urine(80–85%), but, as with d -tubocurarine, some is also excreted in the bile (15–20%) [ ]. Persistent relaxation has been reported in renal insufficiency [ ] and the drug is relatively contraindicated in this condition.
Organs and systems
Cardiovascular
Tachycardia, hypotension, and a fall in total peripheral resistance all occur to an extent similar to that seen with d -tubocurarine, according to most studies [ ]. Others have reported that these effects are short-lived [ ]. Doses of 0.2 mg/kg or more may be associated with the more extreme cardiovascular effects. Blockade of cardiac muscarinic receptors [ ], histamine release, and, possibly, some ganglionic blockade (although it has a very low ganglion-blocking activity in animals) [ ] may all play a role in the production of the cardiovascular effects of alcuronium.
Nervous system
Two patients in intensive care treated with infusions of large amounts of alcuronium developed fixed dilated pupils. Within 6–24 hours after stopping the infusion the pupils became normally reactive again [ ].
This is a very important and dangerous adverse effect, since the presence of fixed dilated pupils may lead to the mistaken diagnosis of brain death in coma patients if other neurological diagnostic procedures are not carried out.
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