Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Mucosal Barrier of the Stomach01:25

Mucosal Barrier of the Stomach

The gastric glands contain parietal cells that secrete hydrochloric acid (HCl) for digestion. The cells secrete HCl because it is highly corrosive and essential for breaking down food. To achieve this, they secrete hydrogen and chloride ions into the lumen of the gastric glands, which combine to form HCl.
Within parietal cells, carbonic acid is first formed through the reaction of water and carbon dioxide. The dissociation of carbonic acid releases bicarbonate and hydrogen ions. The bicarbonate...
Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors01:24

Pathophysiology of Peptic Ulcer Disease: Mucosal Defense Factors

Peptic ulcer disease, commonly called PUD, represents a multifaceted condition characterized by disruptions in the lining of the gastrointestinal (GI)  tract. Central to the protection of the gastrointestinal lining is the mucosal-bicarbonate barrier. This physiological defense mechanism is a formidable shield against the corrosive effects of gastric acid and pepsin secretion in the stomach. Its role is pivotal in maintaining the structural integrity of the stomach's inner lining. Bicarbonate,...
Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists01:28

Acid Suppressive Drugs for Peptic Ulcer Disease: Histamine H2-Receptor Antagonists

Histamine H2 receptors, which are intricately located on the basolateral membrane of parietal cells, play a crucial role in modulating gastric acid secretion. When released from enterochromaffin-like cells, histamine engages H2 receptors, initiating the cyclic AMP (cAMP) pathway. In this pathway, adenylyl cyclase converts ATP into cAMP, elevating intracellular cAMP levels. The activation of protein kinase A follows, stimulating the proton pump. This stimulation prompts the secretion of hydrogen...
Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents01:20

Drugs for Peptic Ulcer Disease: Prostaglandin Analogs as Mucosal Protective Agents

The gastric mucosa produces prostaglandins E2 (PGE2) and prostacyclin (PGI2), crucial in maintaining gastric health. They exert cytoprotective effects, including increasing bicarbonate secretion, releasing protective mucin, reducing gastric acid output, and preventing harmful vasoconstriction. These effects are mediated through various receptors, such as EP1, EP2, EP3, and EP4.
Non-steroidal anti-inflammatory drugs (NSAIDs) can induce peptic ulcers by inhibiting cyclooxygenase, decreasing...
Peptic Ulcer Disease II: Pathophysiology01:24

Peptic Ulcer Disease II: Pathophysiology

Peptic ulcer disease develops when protective mechanisms of the gastrointestinal mucosa are overwhelmed by harmful factors, leading to localized erosions in the stomach or proximal duodenum. The main causes are Helicobacter pylori infection and chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs).Helicobacter pylori–Induced InjuryBacterial Adaptation and Colonization:H. pylori is a spiral, Gram-negative bacterium adapted to the acidic stomach. and transmitted through oral-oral or...
Peptic Ulcer Disease II: Pathophysiology01:28

Peptic Ulcer Disease II: Pathophysiology

Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Tranexamic acid impact on platelet adhesion to the endothelium after shock conditions: A protective effect?

The journal of trauma and acute care surgery·2025
Same author

Detection of glycocalyx degradation in real time: A conceptual model of thromboelastography.

Surgery·2023
Same author

Effect of albumin solutions on endothelial oxidant injury: A microfluidic study.

Surgery·2022
Same author

Effect of tranexamic acid on endothelial von Willebrand factor/ADAMTS-13 response to in vitro shock conditions.

The journal of trauma and acute care surgery·2022
Same author

The effect of tranexamic acid dosing regimen on trauma/hemorrhagic shock-related glycocalyx degradation and endothelial barrier permeability: An in vitro model.

The journal of trauma and acute care surgery·2022
Same author

Plasma components to protect the endothelial barrier after shock: A role for sphingosine 1-phosphate.

Surgery·2021
Same journal

Outcomes following endovascular aortic aneurysm repair in nonagenarian patients.

Surgery·2026
Same journal

Fistulotomy with primary sphincteroplasty for complex anal fistulas: Should we be concerned about incontinence?

Surgery·2026
Same journal

No need for mesh in the repair of hiatal hernias: Autologous tissue hiatoplasty techniques for the repair of the complex diaphragmatic defect.

Surgery·2026
Same journal

Incretin-based therapies and altered myocardial metabolism in a swine model of ischemic heart disease in the setting of metabolic syndrome.

Surgery·2026
Same journal

Colonoscopy utilization and persistent disparities in early onset colorectal cancer: A multistate, multi-institution nested case-control study.

Surgery·2026
Same journal

From blades to heels: Lessons in performance from the ice to the practice of surgery.

Surgery·2026
See all related articles

Related Experiment Video

Updated: May 28, 2026

Three-dimensional Quantification of Intestinal Mucus Using Whole-mount Tissue Imaging
05:10

Three-dimensional Quantification of Intestinal Mucus Using Whole-mount Tissue Imaging

Published on: September 12, 2025

H2 blockers decrease gut mucus production and lead to barrier dysfunction in vitro.

Lawrence N Diebel1, David M Liberati, Lisa Hall-Zimmerman

  • 1Department of Surgery, Wayne State University, Detroit, MI 48201, USA. ldiebel@med.wayne.edu

Surgery
|October 18, 2011
PubMed
Summary
This summary is machine-generated.

Histamine 2 (H2) receptor antagonists like cimetidine reduce mucus production, impairing gut barrier function. This increases the risk of infections in critically ill patients, suggesting H2 blockers may be ill-advised.

More Related Videos

Assessment of Gut Barrier Integrity in Mice Using Fluorescein-Isothiocyanate-Labeled Dextran
05:14

Assessment of Gut Barrier Integrity in Mice Using Fluorescein-Isothiocyanate-Labeled Dextran

Published on: November 18, 2022

Investigating Intestinal Barrier Breakdown in Living Organoids
07:18

Investigating Intestinal Barrier Breakdown in Living Organoids

Published on: March 26, 2020

Related Experiment Videos

Last Updated: May 28, 2026

Three-dimensional Quantification of Intestinal Mucus Using Whole-mount Tissue Imaging
05:10

Three-dimensional Quantification of Intestinal Mucus Using Whole-mount Tissue Imaging

Published on: September 12, 2025

Assessment of Gut Barrier Integrity in Mice Using Fluorescein-Isothiocyanate-Labeled Dextran
05:14

Assessment of Gut Barrier Integrity in Mice Using Fluorescein-Isothiocyanate-Labeled Dextran

Published on: November 18, 2022

Investigating Intestinal Barrier Breakdown in Living Organoids
07:18

Investigating Intestinal Barrier Breakdown in Living Organoids

Published on: March 26, 2020

Area of Science:

  • Gastroenterology
  • Microbiology
  • Pharmacology

Background:

  • Histamine 2 (H2) receptor antagonists are linked to gut infections in critically ill patients.
  • Mechanisms may involve acid suppression, altered gut flora, immunologic effects, or impaired gut barrier function.
  • Mucus plays a critical role in gastrointestinal mucosal barrier integrity.

Purpose of the Study:

  • To investigate the in vitro effects of cimetidine on mucus production.
  • To assess the impact of cimetidine on intestinal mucosal barrier function.

Main Methods:

  • Used HT29-MTX intestinal cells, a mucus-producing cell line.
  • Treated cells with cimetidine for 0, 3, or 6 days.
  • Quantified mucus/mucin content and measured bacterial adherence and passage using Escherichia coli (EC).

Main Results:

  • Cimetidine significantly decreased mucus/mucin content in a time-dependent manner.
  • Bacterial passage across cell monolayers nearly doubled after cimetidine treatment.
  • Mucosal barrier function was compromised by cimetidine exposure.

Conclusions:

  • Cimetidine impairs gut barrier function by reducing mucus production.
  • Findings support clinical concerns regarding the routine use of H2 blockers in critically ill patients.
  • H2 receptor antagonists may increase the risk of gut-related infectious complications.