Neuromuscular blockers nondepolarizing agents

Some of the new fa/s-quaternary ammonium agents produced depolarization of the postjunctional membrane at the neuromuscular junction before causing blockade other compounds, such as tubocurarine, did not produce this depolarization. Thus, the structural features of the remainder of the molecule determined whether the nicotinic antagonist was a depolarizing or a nondepolarizing neuromuscular blocker. 

An ideal neuromuscular blocking agent would be a nondepolarizing compound that is metabolically inactivated and rapidly eliminated. Efforts to design such a neuromuscular blocker have resulted in the development of several synthetic neuromuscular agents. Those that have found clinical use are either aminosteroids derived from (+)-malouetine (an aminosteroid found in the rain forest of central Africa) (Fig. 12.21) or... 

D. When neostigmine or pyridostigmine is used to reverse nondepolarizing neuromuscular blockade, glycopyrrolate is the preferred agent to block unwanted muscarinic effects (neuromuscular blockers, see p 472). 

C. Succinylcholine produces the most rapid onset of effects, with total paralysis within 30-60 seconds after intravenous administration. It is rapidly hydrolyzed by plasma cholinesterases, and its effects dissipate in 10-20 minutes. Rocuronium, a nondepolarizing agent, also offers a rapid onset for rapid sequence intubations. Onset and duration of several other neuromuscular blockers are described in Table III-9. 

A. Neuromuscular blockers are used to abolish excessive muscular activity, rigidity, or peripheral seizure activity when continued hyperactivity may produce or aggravate rhabdomyolysis and hyperthermia. Examples of such situations include the following. Note The preferred agent for these conditions is a nondepolarizing agent. 

D. Anticonvulsants (carbamazepine and phenytoin) and theophylline may delay the onset and shorten the duration of action of some nondepolarizing agents. Carbamazepine has additive effects, and reduction of the neuromuscular blocker dose may be required. 

The effect of administering different botulinum neurotoxin serotypes at the same time or within several months of each other is unknown. Excessive neuromuscular weakness may be exacerbated by administration of another botulinum toxin prior to the resolution of the effects of a previously administered botulinum toxin. Aminoglycosides Cautiously perform coadministration of botulinum toxin type A and aminoglycosides or other agents interfering with neuromuscular transmission (eg, curare-like nondepolarizing blockers, lincosamides, polymyxins, quinidine, magnesium sulfate, anticholinesterases, succinylcholine chloride) because the effect of the toxin may be potentiated. 

Nondepolarizing neuromuscular blocking agent protot3pe competitive nicotinic blocker. Releases histamine and may cause hypotension. Analogs pancuronium, atracurium, vecuronium, and other -curiums and -curoniums. Antidote cholinesterase inhibitor, eg, neostigmine. 

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