Related Experiment Video

Updated: Jul 26, 2026

Mechanisms Underlying Gut Hormone Secretion Using the Isolated Perfused Rat Small Intestine
07:00

Mechanisms Underlying Gut Hormone Secretion Using the Isolated Perfused Rat Small Intestine

Published on: February 26, 2019

Gastrin-mediated effects of omeprazole on rat colon mucosa

M E Klingensmith1, L J Neville, E Delpire

  • 1Department of Surgery, Brigham and Women's Hospital, Boston, Mass., USA.

Surgery
|August 24, 1999
PubMed
Abstract

More Related Videos

Studying the Epithelial Effects of Intestinal Inflammation In Vitro on Established Murine Colonoids06:31

Studying the Epithelial Effects of Intestinal Inflammation In Vitro on Established Murine Colonoids

Published on: June 2, 2023

Effects of Desmodium caudatum on Gastrointestinal Hormones and Intestinal Flora in Rats with Gastritis03:48

Effects of Desmodium caudatum on Gastrointestinal Hormones and Intestinal Flora in Rats with Gastritis

Published on: March 1, 2024

Related Concept Videos

Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds to M3...
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...
Drugs Affecting GI Tract Motility: Serotonin Receptor Agonists01:23

Drugs Affecting GI Tract Motility: Serotonin Receptor Agonists

Serotonin, a crucial neurotransmitter synthesized by enterochromaffin cells, plays a cardinal role in regulating gastrointestinal (GI) motility. With over 90% of the body's total serotonin in the GI tract, its influence on digestive processes is profound. Serotonin is swiftly released upon various stimuli, such as food boluses or certain drugs, triggering intrinsic sensory neurons in the myenteric plexus and extrinsic vagal and spinal sensory neurons. This leads to the activation of the...
Intestinal Phase of Digestion01:29

Intestinal Phase of Digestion

The intestinal phase of digestion is the third and final stage of the digestive process, occurring after the cephalic and gastric phases. It begins when chyme, a partially digested mixture of food and digestive enzymes, enters the small intestine from the stomach. This phase is crucial for nutrient absorption and involves complex hormonal and enzymatic interactions.
The arrival of the chyme in the small intestine distends the duodenum, which triggers the enterogastric reflex. This distension...
Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...