Decamethonium: Difference between revisions
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== Decamethonium == | |||
[[File:Decamethonium.svg|thumb|right|Chemical structure of Decamethonium]] | |||
'''Decamethonium''' is a [[neuromuscular-blocking drug]] that was historically used in [[anesthesia]] to induce [[muscle relaxation]] during [[surgery]]. It is a [[depolarizing neuromuscular blocker]], which means it works by mimicking the action of [[acetylcholine]] at the [[neuromuscular junction]], leading to sustained [[depolarization]] of the [[muscle]] [[membrane]]. | |||
Decamethonium | |||
== | == Mechanism of Action == | ||
== | Decamethonium acts as an [[agonist]] at the [[nicotinic acetylcholine receptor]]s located on the [[motor end plate]] of the [[skeletal muscle]] fibers. By binding to these receptors, it causes an initial [[depolarization]] of the muscle membrane, which is followed by a prolonged [[refractory period]] during which the muscle cannot respond to further stimulation. This results in [[muscle paralysis]]. Unlike [[non-depolarizing neuromuscular blockers]], decamethonium does not have a competitive antagonistic effect but rather causes a persistent depolarization. | ||
Decamethonium was | |||
== Clinical Use == | |||
Decamethonium was primarily used to facilitate [[endotracheal intubation]] and to provide muscle relaxation during [[surgical procedures]]. However, its use has largely been replaced by other neuromuscular blockers with more favorable profiles, such as [[succinylcholine]] and [[rocuronium]]. | |||
== Pharmacokinetics == | |||
Decamethonium is administered [[intravenously]] and has a rapid onset of action. The duration of action is relatively short, which made it suitable for short surgical procedures. It is metabolized by [[plasma cholinesterase]], and its effects are terminated as the drug is broken down and cleared from the body. | |||
== Side Effects == | |||
The use of decamethonium can lead to several side effects, including: | |||
* [[Hyperkalemia]] due to the release of [[potassium]] from muscle cells. | |||
* [[Bradycardia]] or [[tachycardia]] due to autonomic effects. | |||
* [[Malignant hyperthermia]] in susceptible individuals. | |||
* [[Prolonged apnea]] in patients with atypical [[cholinesterase]]. | |||
== History == | |||
Decamethonium was one of the first neuromuscular blockers to be used clinically. It was developed in the mid-20th century and was used extensively until the development of newer agents with fewer side effects and more predictable pharmacokinetics. | |||
== Related Pages == | |||
* [[Neuromuscular-blocking drug]] | * [[Neuromuscular-blocking drug]] | ||
* [[Succinylcholine]] | |||
* [[Rocuronium]] | |||
* [[Anesthesia]] | * [[Anesthesia]] | ||
* [[Acetylcholine]] | * [[Acetylcholine]] | ||
[[Category:Neuromuscular | [[Category:Neuromuscular blockers]] | ||
Latest revision as of 11:49, 15 February 2025
Decamethonium[edit]
Decamethonium is a neuromuscular-blocking drug that was historically used in anesthesia to induce muscle relaxation during surgery. It is a depolarizing neuromuscular blocker, which means it works by mimicking the action of acetylcholine at the neuromuscular junction, leading to sustained depolarization of the muscle membrane.
Mechanism of Action[edit]
Decamethonium acts as an agonist at the nicotinic acetylcholine receptors located on the motor end plate of the skeletal muscle fibers. By binding to these receptors, it causes an initial depolarization of the muscle membrane, which is followed by a prolonged refractory period during which the muscle cannot respond to further stimulation. This results in muscle paralysis. Unlike non-depolarizing neuromuscular blockers, decamethonium does not have a competitive antagonistic effect but rather causes a persistent depolarization.
Clinical Use[edit]
Decamethonium was primarily used to facilitate endotracheal intubation and to provide muscle relaxation during surgical procedures. However, its use has largely been replaced by other neuromuscular blockers with more favorable profiles, such as succinylcholine and rocuronium.
Pharmacokinetics[edit]
Decamethonium is administered intravenously and has a rapid onset of action. The duration of action is relatively short, which made it suitable for short surgical procedures. It is metabolized by plasma cholinesterase, and its effects are terminated as the drug is broken down and cleared from the body.
Side Effects[edit]
The use of decamethonium can lead to several side effects, including:
- Hyperkalemia due to the release of potassium from muscle cells.
- Bradycardia or tachycardia due to autonomic effects.
- Malignant hyperthermia in susceptible individuals.
- Prolonged apnea in patients with atypical cholinesterase.
History[edit]
Decamethonium was one of the first neuromuscular blockers to be used clinically. It was developed in the mid-20th century and was used extensively until the development of newer agents with fewer side effects and more predictable pharmacokinetics.
