Tubocurare and succinylcholine

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  1. Blockade of normal endplate function can occur by two mechanisms: drugs that prevent access of the transmitter to its receptor and prevent depolarization (nondepolarizing group) and drugs that block transmission by producing an excess of depolarizing agonist (depolarizing group - a paradoxical effect that also occurs at the ganglionic nicotinic acetylcholine receptor)
  2. Nondepolarizing (e.g. tubocurare)
    1. rapid initial distribution phase followed by slower elimination
    2. vecuronium has a shorter duration of action than most (20-35 minutes vs. 60 minutes for pancuronium)
    3. rocuronium is similar to vecuronium but has a more rapid onset time
    4. act at nicotinic receptor sites to compete with acetylcholine
    5. rarely causes cardiac arrhythmias
  3. Depolarizing (e.g. succinylcholine – all neuromuscular blocking drugs in use in the United states except succinylcholine are nondepolarizing agents)
    1. extremely brief duration of action (5-10 minutes) because it is rapidly metabolized by the liver
    2. neuromuscular effects are identical to acetylcholine but produces a longer effect; reacts with the nicotinic receptor to open the channel and cause depolarization of the end plate, spreads to other membranes to depolarize them, causing generalized disorganized contraction of muscle motor units
    3. after repolarization, the membrane cannot be depolarized again by acetylcholine as long as succinylcholine is present (membrane is effectively desensitized)
    4. may cause cardiac arrhythmias
    5. may induce hyperkalemia
    6. patients who receive succinylcholine are prone to muscle pain afterward
    7. effects of succinylcholine are not reversed by an anticholinesterase agent
    8. effects may be amplified by decreased muscle temperature
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