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Related Concept Videos

Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action01:17

Nondepolarizing (Competitive) Neuromuscular Blockers: Mechanism of Action

Nondepolarizing neuromuscular blockers induce paralysis by competitively blocking nicotinic acetylcholine receptors at the muscle end plate. Examples include pancuronium, mivacurium, vecuronium, and rocuronium. These quaternary ammonium derivatives are administered intravenously, are poorly absorbed, and are excreted via the kidneys.
Competitive antagonists prevent acetylcholine from binding to its receptor, inhibiting membrane depolarization. Without conformational changes or intrinsic...
Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions01:27

Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions

Nondepolarizing neuromuscular blockers prevent the membrane depolarization of muscle cells and inhibit muscle contraction. These are usually administered with anesthetics to achieve complete muscle relaxation. Upon administration, these drugs first block the small, rapidly contracting muscles of the face and hands, followed by the larger muscles of the trunk and the intercostal muscles. The diaphragm is the last muscle to be affected.
Although all competitive neuromuscular blockers are designed...
Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacokinetics01:11

Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacokinetics

All neuromuscular blocking agents are injected intravenously because they are poorly absorbed from the GI tract. Rapid onset is achieved with intravenous administration, although absorption is also adequate from an intramuscular injection. Since these agents are highly ionized, they do not readily penetrate cell membranes or cross the blood-brain barrier.
Instead, they are transported by the blood to different tissues. Muscles with a greater blood supply (arteries) and blood flow receive more...
Depolarizing Blockers: Mechanism of Action01:28

Depolarizing Blockers: Mechanism of Action

Depolarizing blockers act on skeletal muscle fibers' membranes and induce their depolarization. Most depolarizing blockers have two quaternary N+ atoms that bind the nicotinic acetylcholine receptors and cause neuromuscular blockade within minutes.
Succinylcholine is the most commonly used depolarizing blocker. Chemically, it constitutes two molecules of acetylcholine joined together by an acetate methyl group. They act on the receptors in the same way as acetylcholine. Because succinylcholine...
Neuromuscular Junction And Blockade01:29

Neuromuscular Junction And Blockade

The site of chemical communication between a motor neuron and a muscle fiber is called the neuromuscular junction (NMJ). The end of the motor neuron at the NMJ divides into a cluster of synaptic end bulbs. The cytoplasm of these bulbs consists of synaptic vesicles enclosing acetylcholine molecules, the principal neurotransmitter released at the NMJ. The region opposite the synaptic bulb that ends in the muscle fiber is called the motor end plate, which has acetylcholine receptors. Within the...
Depolarizing Blockers: Pharmocokinetics01:19

Depolarizing Blockers: Pharmocokinetics

Depolarizing blockers are administered through intravenous injection. Succinylcholine is the most common choice of depolarizing blockers in emergency clinical practices. Although they have a rapid onset, they readily diffuse away from the motor end plate into the extracellular fluid. They are metabolized by enzymes such as liver butyrylcholinesterase and plasma pseudocholinesterases. This produces a short duration of action, typically 5-10 minutes long, unlike nondepolarizing blockers, which...

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Stimulated Single Fiber Electromyography (SFEMG) for Assessing Neuromuscular Junction Transmission in Rodent Models
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Sugammadex: a novel neuromuscular blocker binding agent.

Aaron M Fields1, Nalini Vadivelu

  • 1Department of Anesthesiology, Yale University School of Medicine, New Haven, CT 06520-8051, USA. afieldsmd@gmail.com

Current Opinion in Anaesthesiology
|July 11, 2007
PubMed
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Sugammadex offers a new way to reverse neuromuscular blockade, potentially changing anesthesia delivery. This drug is safe and effective, with availability pending FDA approval.

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Area of Science:

  • Anesthesiology
  • Pharmacology

Background:

  • Sugammadex is a novel drug designed to bind and inactivate neuromuscular blocking agents.
  • It acts by encapsulating these drugs, preventing their action at the neuromuscular junction.

Purpose of the Study:

  • To review the existing literature on sugammadex.
  • To discuss the potential impact of sugammadex on anesthesia practices.

Main Methods:

  • Literature review of studies on sugammadex.
  • Analysis of clinical trial data regarding safety and efficacy.

Main Results:

  • Sugammadex has demonstrated safety and efficacy in preclinical and early clinical studies.
  • Phase III trials are ongoing to support FDA approval for widespread use.

Conclusions:

  • Sugammadex effectively reverses neuromuscular blockade, rendering cholinesterase inhibitors potentially obsolete.
  • Its rapid action allows for prolonged muscle relaxation and swift return to spontaneous ventilation, even in critical scenarios.
  • Further information on cost and availability is pending.