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Depolarizing Blockers: Pharmocokinetics01:19

Depolarizing Blockers: Pharmocokinetics

419
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...
419
Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions01:27

Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions

654
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...
654
Parenteral Anesthetics: Overview01:24

Parenteral Anesthetics: Overview

350
Intravenous anesthetics are drugs administered parenterally to induce anesthesia or sedation. Propofol is a widely used agent formulated as a 1% emulsion in soybean oil, glycerol, and egg phosphatide. It induces rapid anesthesia primarily due to its rapid distribution from the bloodstream to target tissues and is metabolized in the liver. However, it can cause significant pain on injection and hypertriglyceridemia. Fospropofol, a water-based prodrug of propofol, lacks these adverse effects.
350
Skeletal Muscle Relaxants: Adverse Effects01:21

Skeletal Muscle Relaxants: Adverse Effects

544
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...
544
Depolarizing Blockers: Mechanism of Action01:28

Depolarizing Blockers: Mechanism of Action

2.1K
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...
2.1K
Cardiopulmonary Resuscitation IV: Pharmacological Management01:25

Cardiopulmonary Resuscitation IV: Pharmacological Management

144
Pharmacologic intervention is crucial in treating cardiac arrest patients during ACLS or Advanced Cardiovascular Life Support. The ACLS algorithms guide the administration of specific drugs based on the patient's cardiac arrest rhythm, which includes pulseless ventricular tachycardia (VT), ventricular fibrillation (VF), asystole, and pulseless electrical activity (PEA).EpinephrineIndication: Epinephrine is the first-line drug for all cardiac arrest rhythms.Mechanism of Action: Epinephrine...
144

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Related Experiment Video

Updated: Oct 26, 2025

Acquisition of Resting-State Functional Magnetic Resonance Imaging Data in the Rat
12:41

Acquisition of Resting-State Functional Magnetic Resonance Imaging Data in the Rat

Published on: August 28, 2021

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Dexmedetomidine may decrease the bupivacaine toxicity to heart.

Zhousheng Jin1, Fangfang Xia2, Tingting Lin2

  • 1Department of Anesthesiology and Perioperative Medicine, Shandong Qianfoshan Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong Province, 250014, China.

Open Medicine (Warsaw, Poland)
|July 26, 2021
PubMed
Summary

Dexmedetomidine reduces bupivacaine-induced cardiotoxicity by decreasing endothelial cell permeability. This effect is mediated by increased Zonula occludens-1 (ZO-1) and the PI3K/Akt pathway, suggesting a protective role for dexmedetomidine.

Keywords:
PI3K/Akt pathwayZO-1bupivacainecardiac tolerancedexmedetomidine

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Area of Science:

  • Cardiovascular Pharmacology
  • Cellular Biology
  • Anesthesiology

Background:

  • Bupivacaine can induce cardiotoxicity, potentially by increasing vascular permeability.
  • Dexmedetomidine is an alpha-2 adrenergic agonist with potential cardioprotective effects.
  • Understanding the interaction between dexmedetomidine and bupivacaine is crucial for safe anesthetic practices.

Purpose of the Study:

  • To investigate the effect of dexmedetomidine on cardiac tolerance to bupivacaine.
  • To elucidate the underlying cellular mechanisms involved in this interaction.

Main Methods:

  • An in vitro model using human coronary endothelial cells was established.
  • Cells were treated with dexmedetomidine, bupivacaine, or both, with and without a PI3K inhibitor.
  • Cell activity, permeability, and protein expression (ZO-1, PI3K, Akt, PTEN) were assessed.

Main Results:

  • Dexmedetomidine significantly reduced bupivacaine-induced endothelial cell permeability.
  • This protective effect was associated with increased Zonula occludens-1 (ZO-1) expression.
  • The mechanism involved the PI3K/Akt pathway, as indicated by increased PI3K and p-Akt levels, and was blocked by PI3K inhibitors.

Conclusions:

  • Dexmedetomidine mitigates bupivacaine-induced vasopermeability via ZO-1 and the PI3K/Akt pathway.
  • This action may contribute to decreased bupivacaine-induced cardiotoxicity.
  • Dexmedetomidine shows potential as a protective agent against bupivacaine cardiotoxicity.