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some info i got googling!!

Mechanism of action of succinyl choline:

phase 1 block

  • Binding of suxamethonium to the nicotinic acetylcholine receptor results in opening of the receptor's nicotinic sodium channel; sodium moves into the cell, a disorganised depolarisation of the motor end plate occurs and calcium is released from the sarcoplasmic reticulum. This results in fasciculation.
  • In the normal muscle, following depolarisation, acetylcholine is rapidly hydrolysed by acetylcholinesterase and the muscle cell is able to 'reset' ready for the next signal.
  • Suxamethonium has a longer duration of effect than acetylcholine and is not hydrolysed by acetylcholinesterase. It does not allow the muscle cell to 'reset' and keeps the 'new' resting membrane potential below threshold. When acetylcholine binds to an already depolarised receptor it cannot cause further depolarisation.
  • Calcium is removed from the muscle cell cytosol independent of repolarisation (depolarization signalling and muscle contraction are independent processes). As the calcium is taken up by the sarcoplasmic reticulum, the muscle relaxes. This explains muscle flaccidity rather than tetany following fasciculation.

phase 2 block

  • Following infusion or repeated doses of suxamethonium, phase 2 block may occur.
  • The receptor blockade takes on characteristics of a non-depolarising neuromuscular block (ie. fade in response to nerve stimulation, however unlike non-depolarizing neuromuscular blocking agents it cannot be reversed
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