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Nondepolarizing (Competitive) Neuromuscular Blockers: Pharmacological Actions01:27

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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.
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Indirect-acting cholinergic agonists, also known as anticholinesterases, exert their pharmacological effects by enhancing cholinergic transmission in various body parts, including the neuromuscular junction, autonomic cholinergic synapses, and the brain.
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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.
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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.
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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.
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Esophageal Strictures-I: Introduction01:30

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Esophageal strictures involve abnormal narrowing or tightening of the esophagus. They vary in length and severity, ranging from mild constriction to complete obstruction, and are classified as benign (noncancerous) or malignant (cancerous).
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Esophageal hypercontractility is abolished by cholinergic blockade.

Arash Babaei1,2, Sadaf Shad1, Benson T Massey1

  • 1Division of Gastroenterology and Hepatology, Medical College of Wisconsin, Milwaukee, WI, USA.

Neurogastroenterology and Motility
|November 13, 2020
PubMed
Summary

Esophageal hypercontractility (EHC) is driven by cholinergic hyperactivity, not loss of inhibition. Most EHC patients may benefit from anticholinergic treatments targeting excessive nerve signaling.

Keywords:
achalasiahigh-resolution manometryjackhammer esophagusnutcracker esophagusopioid-induced peristalsis disorderoutflow obstruction

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Area of Science:

  • Gastroenterology
  • Esophageal Physiology
  • Neurogastroenterology

Background:

  • Esophageal hypercontractility (EHC) is a significant esophageal motor disorder with an unknown cause.
  • Proposed mechanisms include an imbalance in esophageal innervation.
  • This study investigates if EHC patients experience cholinergic hyperactivity.

Purpose of the Study:

  • To examine excitatory and inhibitory neurotransmission in EHC.
  • To assess esophageal motor responses to atropine (ATR) and cholecystokinin (CCK) in EHC patients.

Main Methods:

  • Retrospective review of 49 EHC patients undergoing high-resolution manometry (HRM) with pharmacologic challenge (2007-2017).
  • Patients categorized by hypercontractile peristaltic sequence frequency.
  • Analysis of pressure metrics and motor responses to IV ATR and CCK.

Main Results:

  • Atropine administration eliminated hypercontractility in all studied groups.
  • Nearly half of patients showed ineffective esophageal motility post-atropine.
  • Abnormal CCK responses were mainly observed in patients with concurrent outflow obstruction.

Conclusions:

  • Esophageal hypercontractility is mediated by cholinergic pathways.
  • Isolated EHC is primarily linked to excessive cholinergic drive, not impaired inhibitory innervation.
  • EHC patients may be suitable candidates for anticholinergic therapies.