Neuromuscular blocking action of suxamethonium after antagonism of vecuronium by edrophonium, pyridostigmine or neostigmine

Abstract

The reported effects of edrophonium on a subsequent dose of suxamethonium are variable and the effects of pyridostigmine have not been evaluated extensively. We have studied this interaction in patients anaesthetized with propofol and sufentanil. After recovery from an initial bolus (1 mg kg-1) of suxamethonium, vecuronium was infused to produce 75% block. After 30 min, the infusion was discontinued and saline 5 ml, edrophonium 0.75 mg kg-1, pyridostigmine 0.24 mg kg-1 or neostigmine 0.05 mg kg-1 was given. Fifteen minutes later the mean durations of a second bolus of suxamethonium were: 10.5 (SD 3.9) min (saline), 10.9 (3.7) min (edrophonium), 18.7 (5.4) min (pyridostigmine) and 23.8 (7.4) min (neostigmine). Corresponding plasma cholinesterase activities (percentage of baseline) were: 91 (18), 87 (9), 21 (10) and 52 (26). When both treatment groups and individual patients were compared, the changes in duration of action did not correlate with changes in cholinesterase activity. These data suggest that other mechanisms in addition to cholinesterase inhibition may contribute to this drug interaction.

Butyrylcholinesterase deficiency and its clinical importance in anaesthesia: a systematic review

“…Butyrylcholinesterase activity is reduced even more by pyridostigmine, but succinylcholine blockade is prolonged by a moderate 4–5 min . Edrophonium does not affect the butyrylcholinesterase activity and when given after mivacurium shortens neuromuscular blockade by 4–8 min, compared with neostigmine .…”

“…Neostigmine reduces butyrylcholinesterase activity and prolongs the action of succinylcholine and mivacurium by 7–9 min and 40 min, respectively, when given before succinylcholine or mivacurium . However, this action is not seen when neostigmine is given after succinylcholine or mivacurium .…”

“…and Table ). Butyrylcholinesterase deficiency prolongs succinylcholine and mivacurium neuromuscular blockade by minutes (mins) to hours, measured by: neuromuscular stimulation, using either mechanomyogram or electromyography with train‐of‐four stimulation ; single twitch stimulation or tactile monitoring or by ventilatory status or muscle strength . In genotypically normal adults the duration of succinylcholine or mivacurium neuromuscular blockade is proportionate to butyrylcholinesterase deficiency .…”

Concurrent medication and the neuromuscular junction

“…Reduced metabolism of the depolarizing drugs results in a propensity for prolonged recovery and the development of phase 2 block [112]. There does, however, seem to be little correlation between plasma cholinesterase activity and the duration of block [113].…”

Dibucaine Inhibition of Serum Cholinesterase

“…However, SChE was found useful in terminating the neuromuscular block of the muscle relaxants suxamethonium and mivacurium. It hydrolyses these compounds which are sometimes used in clinical anesthesia to facilitate intubation or other medical procedures (Goedde et at., 1968;Hersh et al, 1974;Cook et al, 1989;Ostergard et al, 1992;Fleming et al, 1996). However, some patients were suxamethonium-sensitive and quantitatively low in SChE activity, a geneticallydetermined property (Kalow and Genest, 1957;Thompson and Wittaker, 1966;Hobbiger and Peck, 1969;VibyMogensen, 1981;Cattozzo et al, 1993;Mitchell and HarropGriffiths, 1994;Sockalingam and Green, 1995).…”