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Related Concept Videos

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: 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...
Skeletal Muscle Relaxants: Adverse Effects01:21

Skeletal Muscle Relaxants: Adverse Effects

Skeletal muscle relaxants are widely used for muscle paralysis and relieving pain following any muscle injury or stiffness. However, depending on the drug type, they can have adverse effects that range from mild to severe. Usually, nondepolarizing neuromuscular blockers have minimal side effects. For example, drugs like d-tubocurarine, cisatracurium, and rocuronium cause hypotension, whereas drugs like baclofen, when stopped abruptly, can lead to the recurrence of spastic conditions.
Unlike...
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...
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...

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Related Experiment Video

Updated: Jun 28, 2026

Stimulated Single Fiber Electromyography (SFEMG) for Assessing Neuromuscular Junction Transmission in Rodent Models
04:30

Stimulated Single Fiber Electromyography (SFEMG) for Assessing Neuromuscular Junction Transmission in Rodent Models

Published on: March 8, 2024

Hypersensitivity reactions to neuromuscular blocking agents.

P M Mertes1, I Aimone-Gastin, R M Guéant-Rodriguez

  • 1Département d'Anesthésie-réanimation, CHU de Nancy, Hôpital Central, 29 Avenue de Lattre de Tassigny, 54035 Nancy Cedex, France. pm.mertes@chu-nancy.fr

Current Pharmaceutical Design
|November 11, 2008
PubMed
Summary

Neuromuscular blocking agents cause hypersensitivity reactions during anesthesia, often IgE-mediated. Allergy assessment is crucial for high-risk patients, investigating suspected drugs and cross-reactivity to ensure future anesthetic safety.

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Basophil Activation Test for Allergy Diagnosis
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Basophil Activation Test for Allergy Diagnosis

Published on: May 31, 2021

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Stimulated Single Fiber Electromyography (SFEMG) for Assessing Neuromuscular Junction Transmission in Rodent Models
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Published on: March 8, 2024

Subcutaneous Administration of Muscarinic Antagonists and Triple-Immunostaining of the Levator Auris Longus Muscle in Mice
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Basophil Activation Test for Allergy Diagnosis
07:22

Basophil Activation Test for Allergy Diagnosis

Published on: May 31, 2021

Area of Science:

  • Anesthesiology
  • Clinical Immunology
  • Pharmacology

Background:

  • Neuromuscular blocking agents (NMBAs) are primary causes of immediate hypersensitivity reactions during anesthesia.
  • These reactions are predominantly IgE-mediated allergies, with incidence varying globally.
  • Potential sensitization mechanisms involve substituted ammonium ions, possibly from environmental sources like pholcodine.

Purpose of the Study:

  • To investigate the mechanisms and diagnostic approaches for hypersensitivity reactions to NMBAs.
  • To evaluate the clinical distinction between IgE-mediated and non-IgE-mediated reactions.
  • To guide the management and prevention of anaphylaxis in anesthesia.

Main Methods:

  • Combined pre- and postoperative testing for suspected hypersensitivity reactions.
  • Intradermal skin testing with all available NMBAs to identify causative agents and cross-reactivity.
  • Basophil activation investigations, including leukocyte histamine release and flow cytometry, for cross-sensitization analysis.

Main Results:

  • Allergic reactions to NMBAs cannot be reliably distinguished from non-IgE-mediated reactions clinically.
  • Frequent, though not systematic, cross-reactivity exists among NMBAs, necessitating comprehensive testing.
  • No evidence supports routine pre-operative screening, but high-risk patients require allergy assessment.

Conclusions:

  • Comprehensive allergy assessment, including skin and basophil activation tests, is vital for patients experiencing suspected hypersensitivity to NMBAs.
  • Identifying causative agents and cross-reactivity patterns is essential for selecting safe anesthetic agents for future procedures.
  • Establishing dedicated allergo-anesthesia centers is recommended to manage patients at risk and provide expert support.