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Updated: Aug 18, 2026

Ex Vivo Intestinal Sacs to Assess Mucosal Permeability in Models of Gastrointestinal Disease
Published on: February 9, 2016
Effect of parental aspirin on the gastric mucosal barrier in the rat
Insights
Parenteral aspirin causes gastric mucosal lesions in rats. Lesions appear before significant disruption of the gastric mucosal barrier, suggesting barrier disruption is a consequence, not the cause, of aspirin-induced injury.
Area of Science:
- Gastroenterology
- Pharmacology
- Toxicology
Background:
- Aspirin is known to cause gastric mucosal injury.
- The mechanism involves disruption of the gastric mucosal barrier to hydrogen ion back-diffusion.
Purpose of the Study:
- To investigate if parenteral aspirin injures the gastric mucosa by disrupting the gastric mucosal barrier.
- To determine the temporal relationship between lesion formation and barrier disruption.
Main Methods:
- Rats were administered sodium acetylsalicylate intraperitoneally.
- Gastric mucosal lesions were scored.
- Back-diffusion studies, including ion fluxes and lumenal potential difference, were conducted at 0.5 and 4 hours post-administration.
Main Results:
- Gastric mucosal lesions developed by 0.5 hours after aspirin administration.
- The gastric mucosal barrier remained intact at 0.5 hours.
- By 4 hours, lesions were more severe, accompanied by a fall in potential difference and increased hydrogen ion loss, indicating barrier disruption.
Conclusions:
- In this rat model, gastric mucosal lesions occur before evidence of diffuse barrier disruption.
- Diffuse barrier disruption is a consequence, not the initial cause, of aspirin-induced gastric mucosal injury.
Abstract:
The purpose of the present study was to determine in the rat whether parenteral aspirin, like topical aspirin, injures the gastric mucosa by diffusely disrupting the gastric mucosal barrier to hydrogen ion back-diffusion. Back-diffusion studies, including the ion fluxes and lumenal potential difference, were performed in control situations and either 0.5 or 4 h after the intraperitoneal administration of sodium acetylsalicylate. Gastric mucosal lesions were scored. After 0.5h, lesions developed but the barrier was intact. However, after 4 h, lesion formation was more severe and changes characteristic of diffuse barrier disruption, fall in potential difference and increased loss of hydrogen ion occurred. Since lesions occurred before evidence of diffuse barrier disruption could be detected, we conclude that in the present model diffuse barrier disruption is a consequence rather than a cause of lesions.
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