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Rocuronium acts by competing for cholinergic receptors at the motor end-plate. This action is antagonized by acetylcholinesterase inhibitors, such as neostigmine and edrophonium. Rocuronium acts by competitively binding to nicotinic cholinergic receptors. The binding of vecuronium decreases the opportunity for acetylcholine to bind to the nicotinic receptor at the postjunctional membrane of the myoneural junction. As a result, depolarization is prevented, calcium ions are not released and muscle contraction does not occur. Evidence also suggests that nondepolarizing agents can affect ACh release. It has been hypothesized that nondepolarzing agents bind to postjunctional (“curare”) receptors and may therefore interfere with the sodium and potassium flux, which is responsible for depolarization and repolarization of the membranes involved in muscle contraction.
Neuromuscular blocking agents are drugs that cause skeletal muscle relaxation primarily by causing a decreased response to the neurotransmitter acetylcholine (ACh) at the myoneural (neuromuscular) junction of skeletal muscle. At that site, ACh normally produces electrical depolarization of the postjunctional membrane of motor end-plate, which leads to conduction of muscle action potential and subsequently induces skeletal muscle contraction. Neuromuscular agents are classified as depolarizing or nondepolarizing. Rocuronium is a nondepolarizing neuromuscular blocking agent with a rapid to intermediate onset depending on dose and intermediate duration. Rocuronium, like vecuronium is longer acting in infants than in children. However, unlike vecuronium, rocuronium retains the characteristics of an intermediate-acting NMBD in infants.
Rocuronium is metabolized to a less active metabolite, 17-desacetyl-rocuronium, and is eliminated primarily by the liver.
No cases of significant accidental or intentional overdose have been reported. Overdosage with neuromuscular blocking agents may result in neuromuscular block beyond the time needed for surgery and anesthesia.
Agoston S, Vandenbrom RH, Wierda JM: Clinical pharmacokinetics of neuromuscular blocking drugs. Clin Pharmacokinet. 1992 Feb;22(2):94-115. [PubMed:1551294]
Khuenl-Brady KS, Sparr H: Clinical pharmacokinetics of rocuronium bromide. Clin Pharmacokinet. 1996 Sep;31(3):174-83. [PubMed:8877248]
Alvarez-Gomez JA: [Rocuronium]. Rev Esp Anestesiol Reanim. 1997 Oct;44(8):310-4. [PubMed:9424684]
Wicks TC: The pharmacology of rocuronium bromide (ORG 9426). AANA J. 1994 Feb;62(1):33-8. [PubMed:8122487]
Sparr HJ, Beaufort TM, Fuchs-Buder T: Newer neuromuscular blocking agents: how do they compare with established agents? Drugs. 2001;61(7):919-42. [PubMed:11434449]
Hemmerling TM, Russo G, Bracco D: Neuromuscular blockade in cardiac surgery: an update for clinicians. Ann Card Anaesth. 2008 Jul-Dec;11(2):80-90. [PubMed:18603747]
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