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Related Concept Videos

Skeletal Muscle Relaxants: Therapeutic Uses01:31

Skeletal Muscle Relaxants: Therapeutic Uses

Skeletal muscle relaxants are used to relax muscle tone and alleviate painful muscle contractions. However, the choice of skeletal muscle relaxants depends on the duration of the surgical procedure in order to minimize potential side effects. Skeletal muscle relaxants like neuromuscular blocking agents [NMBAs] are commonly employed as adjuvants alongside general anesthetics in clinical settings. NMBAs are also used to maintain controlled ventilation during surgery of the larynx or pharynx as...
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...
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...
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...
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 12, 2026

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

Published on: March 8, 2024

Pretreatment with nafamostat mesilate, a kallikrein inhibitor, to decrease withdrawal response associated with

Yoon Hee Kim1, Young Kwon Go, Jung Un Lee

  • 1Department of Anesthesiology and Pain Medicine, Chungnam National University Hospital, 640 Daesa-dong, Jung-gu, Daejeon, 301-721, Korea. yhkim0404@cnu.ac.kr

Journal of Anesthesia
|May 26, 2010
PubMed
Summary
This summary is machine-generated.

Nafamostat mesilate, a kallikrein inhibitor, significantly reduced withdrawal responses to rocuronium injections in a clinical trial. This finding suggests a potential preventive strategy for this common anesthetic side effect.

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Operant Procedures for Assessing Behavioral Flexibility in Rats
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Operant Procedures for Assessing Behavioral Flexibility in Rats

Published on: February 15, 2015

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Last Updated: Jun 12, 2026

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

Published on: March 8, 2024

Operant Procedures for Assessing Behavioral Flexibility in Rats
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Operant Procedures for Assessing Behavioral Flexibility in Rats

Published on: February 15, 2015

Area of Science:

  • Anesthesiology
  • Pharmacology

Background:

  • Rocuronium injection can cause withdrawal responses, a common side effect during anesthesia.
  • Kallikrein inhibitors are being investigated for their potential to mitigate such responses.

Purpose of the Study:

  • To evaluate the preventive effect of nafamostat mesilate on rocuronium-induced withdrawal responses.
  • To assess nafamostat mesilate as a potential prophylactic agent against neuromuscular blockade side effects.

Main Methods:

  • A randomized, double-blind, placebo-controlled study involving 90 patients.
  • Patients received either nafamostat mesilate or a placebo before rocuronium administration.
  • Withdrawal responses, activated coagulation time, and plasma potassium levels were measured.

Main Results:

  • Nafamostat mesilate significantly reduced the incidence of withdrawal response (24.4%) compared to placebo (68.9%).
  • Generalized movement in response to rocuronium was substantially lower in the nafamostat group.
  • No significant changes in potassium levels or activated coagulation time were observed.

Conclusions:

  • Pretreatment with nafamostat mesilate effectively decreases withdrawal responses to rocuronium injection.
  • Nafamostat mesilate shows promise as a preventive measure for rocuronium-induced side effects.