Neuromuscular blockers, competitive,

Neostigmine preceded by atropine to block muscarinic effects rapidly reverses muscle paralysis induced by competitive neuromuscular blockers (decurarization). 

C. This drug may potentiate competitive neuromuscular blockers (see p 472). 

The competitive (non-depolarising) neuromuscular blockers and depolarising neuromuscular blockers mentioned in this section are listed in Table 5.2 , (p.91). The modes of action of the two types of neuromuscular blocker are discussed in the monograph Neuromuscular blockers + Neuromuscular blockers , p.l28. It should be noted that mivacurium (a competitive blocker) and suxamethonium (a depolarising blocker) are hydrolysed by cholinesterase, so share some interactions in common that are not relevant to other competitive neuromuscular blockers. 

The neuromuscular blockade due to suxamethonium (succinyl-choline) can be increased and prolonged by lidocaine, procaine and possibly procainamide. These local anaesthetics all have some neuromuscular blocking activity and may theoretically also enhance the block produced by competitive neuromuscular blockers. Increased toxicity occurred when mivacurium and prilocaine were given together for regional anaesthesia. 

Lidocaine, procaine and procainamide all have some neuromuscular blocking activity and may also enhance the block produced by competitive neuromuscular blockers if given in sufficient doses. However, again, there seems to be an absence of reports of this, probably because the amount of local anaesthetic absorbed into the circulation following a local block is usually modest. ... 

Anticholinesterases oppose the actions of competitive neuromuscular blockers (e.g. tubocurarine) and can therefore be used as an antidote to restore muscular activity following their use. Conversely, anticholinesterases increase and prolong the actions of the depolarising neuromuscular blockers (e.g. suxamethonium (succinylcholine)). Anticholinesterases used to treat Alzheimer s disease may also interact with neuromuscular blockers. 

The effects of many competitive neuromuscular blockers are reduced and shortened if carbamazepine or phenytoin are given for longer than one week, but they appear to be increased if phenytoin, and possibly carbamazepine, are given acutely (e.g. during surgery). Carbamazepine and phenytoin appear not to interact with mivacurium. 

An in vitro study found that the acute neuromuscular effects of carbamazepine reduced the concentrations required for 50% paralysis with both a depolarising neuromuscular blocker (suxamethonium (succinylcholine)) and a competitive neuromuscular blocker (atracurium) by about 30%. ... 

The effects of cisatracurium, mivacurium, pancuronium, rocuro-nium, tubocurarine, vecuronium, and probably other competitive neuromuscular blockers can be increased and prolonged by magnesium sulfate given parenterally. There is some evidence that magnesium may interact similarly with suxamethonium (succinylcholine), but also evidence from well-controlled trials that it does not. 

The interaction between competitive (non-depolarising) neuromuscular blockers and parenteral magnesium is established. Magnesium may decrease the time to onset (vecuronium but not rocuronium), prolong the duration of action and reduce the dose requirement of competitive neuromuscular blockers. Be alert for an increase in the effects of any compet-... 

Suxamethonium and decamethonium would be expected to antagonise competitive neuromuscular blockers due to their opposite mechanisms of action (suxamethonium and decamethonium exert a receptor agonist-type activity whereas competitive blockers exhibit receptor antagonism). However, the depolarising blockers may also reverse a competitive block by enhancing the effect of acetylcholine postsynaptically. ... 

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