Magnesium and Calcium
Magnesium sulfate, given for the treatment of preeclampsia and
eclamptic toxemia, potentiates the neuromuscular block induced by nondepolarizing
neuromuscular blockers.[495]
[496]
[497]
[498]
[499]
[500]
After a dose of 40 mg/kg magnesium sulfate,
the ED50
of vecuronium was reduced by 25%, onset time was nearly halved,
and recovery time just about doubled.[497]
Neostigmine-induced
recovery is also attenuated in patients treated with magnesium.[498]
[501]
The mechanisms underlying the enhancement
of nondepolarizing blockade by magnesium probably involve both prejunctional and
postjunctional effects. High magnesium concentrations inhibit calcium channels at
presynaptic nerve terminals that trigger the release of acetylcholine.[17]
Furthermore, magnesium ions have an inhibitory effect on postjunctional potentials
and cause
a decrease in muscle fiber membrane excitability.[502]
In patients receiving magnesium, the dose of nondepolarizing neuromuscular blocker
must be reduced and carefully titrated by a nerve stimulator to ensure adequate recovery
of neuromuscular function at the end of surgery.
The interaction of magnesium with succinylcholine is controversial.
Initial studies suggested potentiation of depolarizing blockade[503]
or no significant effect.[504]
However, one study
suggests that magnesium may antagonize the block produced by succinylcholine.[505]
Calcium triggers acetylcholine release from the motor nerve terminal
and enhances excitation-contraction coupling in muscle.[17]
Increasing calcium concentrations decreased the sensitivity to dTc and pancuronium
in a muscle-nerve model.[506]
In hyperparathyroidism,
hypercalcemia is associated with decreased sensitivity to atracurium and a shortened
time course of neuromuscular blockade.[507]
