Rocuronium

529.8 g/mol

529.40053318 g/mol

WRE554RFEZ

DTXSID6048339

59 Ų

Complete|2.84e-05 g/L

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.

Approximately 30% bound to human plasma proteins.

For inpatients and outpatients as an adjunct to general anesthesia to facilitate both rapid sequence and routine tracheal intubation, and to provide skeletal muscle relaxation during surgery or mechanical ventilation.

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.

Drugs that interrupt transmission at the skeletal neuromuscular junction without causing depolarization of the motor end plate. They prevent acetylcholine from triggering muscle contraction and are used as muscle relaxants during electroshock treatments, in convulsive states, and as anesthesia adjuvants. (See all compounds classified as Neuromuscular Nondepolarizing Agents.)

Poorly absorbed from the GI tract.|Studies of distribution, metabolism, and excretion in cats and dogs indicate that rocuronium is eliminated primarily by the liver.|0.3 L/kg [3 to <12 mos]|0.25 L/kg/hr [Adults (Ages 27 to 58 years)]

Rocuronium is metabolized to a less active metabolite, 17-desacetyl-rocuronium, and is eliminated primarily by the liver.

The rapid distribution half-life is 1-2 minutes and the slower distribution half-life is 14-18 minutes. Renal impairment has no net effect on half-life, however, half-life is almost doubled in patients with impaired liver function.

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.

1-(17-(acetoyl)-3-hydroxy-2-(4-morpholinyl)androstan-16-yl)-1-(2-propenyl)pyrrolidinium