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Acute acid exposure increases rabbit esophageal cell proliferation
D R Carpizo1, A J Reaka, W R Glaws
1University of Illinois at Chicago, Section of Digestive and Liver Diseases, and the Veterans Affairs Westside Medical Center, 60612-7323, USA.
The Journal of Laboratory and Clinical Medicine
|March 6, 1998
Summary
Acute acid exposure in rabbits significantly increased esophageal cell proliferation, indicated by bromodeoxyuridine (BrDu) labeling and ornithine decarboxylase (ODC) activity. This suggests esophageal acidification acts as a mitogen, even without apparent cell injury.
Area of Science:
- Gastroenterology
- Cell Biology
- Esophageal Physiology
Background:
- Esophageal mucosal injury can lead to cellular changes.
- The role of acid in esophageal cell proliferation requires further investigation.
Purpose of the Study:
- To determine if acute hydrochloric acid (HCl) infusion in rabbits increases esophageal cellular proliferation independently of visible cell injury.
- To investigate the temporal relationship between acid exposure, cell proliferation markers, and esophageal structural changes.
Main Methods:
- Infusion of 40 mmol/L HCl or normal saline (control) into the distal esophagus of rabbits for 1 hour.
- Assessment of cellular proliferation using bromodeoxyuridine (BrDu) labeling and ornithine decarboxylase (ODC) enzyme activity at 24 and 48 hours post-infusion.
- Histological examination for evidence of cell injury and measurement of rete peg prominence.
Main Results:
- A significant increase in BrDu-labeled basal cell nuclei (31% vs. 15% in controls) and threefold higher ODC enzyme activity were observed 24 hours after HCl infusion.
- No gross or microscopic evidence of cell necrosis or inflammation was present at 24 hours.
- Rete peg prominence significantly increased by 48 hours after acid infusion (22 vs. 4 per 100 microm in controls).
Conclusions:
- Acute esophageal acid exposure stimulates mucosal proliferation even in the absence of overt cell injury.
- Esophageal cell acidification may act as a direct or indirect mitogen, promoting cell division.
- These findings highlight a potential mechanism for esophageal changes following acid reflux events.