Mode of action

• Suxamethonium is structurally related to acetylcholine and causes initial stimulation of muscular contraction seen clinically as fasciculation. During this process, the continued stimulation leads to desensitisation of the post-synaptic membrane of the neuromuscular junction with efflux of potassium ions. Subsequent flaccid paralysis is short acting (2-3min) and cannot be reversed (is actually potentiated) by anticholinesterase drugs. Prolonged effects are seen where there is congenital or acquired pseudocholinesterase deficiency.

• Non-depolarising muscle relaxants prevent acetylcholine from depolarising the post-synaptic membrane of the neuromuscular junction by competitive blockade. Reversal of paralysis is achieved by anticholinesterase drugs such as neostigmine. They have a slower onset and longer duration of action than the depolarising agents.

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