Non-depolarising muscle relaxants act at the neuromuscular junction to compete with acetylcholine for its postsynaptic binding site. They do not stimulate ion channel opening and hence cannot initiate end plate firing potentials. A flaccid paralysis results.
Non-depolarising blockers produce a sustained paralysis and as such, they are suited to prolonged operations and the facilitation of IPPV in ventilated patients. Their effect can be reversed with anticholinesterases which shift the equilibrium in favour of cholinergic transmission by increasing the postsynaptic transmitter concentration.
There is a wide range of competitive blocker with different pharmacokinetics and side effects. They are all given by intravenous injection and do not cross the blood-brain barrier. They should be avoided in myasthenia gravis.
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