Gastric lesions induced by concentrated ethanol are associated with a decrease in gastric calcitonin gene-related...

Area of Science:

• Gastroenterology
• Neuroscience
• Pharmacology

Background:

• Ethanol-induced gastric lesions are a significant clinical concern.
• Calcitonin gene-related peptide (CGRP) is a neuropeptide involved in various physiological processes, including gastrointestinal function.
• The specific role of CGRP in acute ethanol-induced gastric injury remains incompletely understood.

Purpose of the Study:

• To investigate the effect of different ethanol concentrations on gastric CGRP-like immunoreactivity (CGRP-li) in rats.
• To determine the specific gastric layer affected by ethanol-induced CGRP-li changes.
• To explore the involvement of capsaicin-sensitive nerves in ethanol-induced CGRP-li depletion.

Main Methods:

• Rats were treated with varying concentrations of ethanol (50%, 75%, 96%).
• Gastric lesions and CGRP-li were assessed at different time points.
• Capsaicin pretreatment was used to deplete CGRP from sensory nerves.

Main Results:

• Ethanol concentrations of 75% and 96% significantly decreased gastric CGRP-li, with lesion severity correlating with ethanol concentration.
• The decrease in CGRP-li was primarily observed in the muscular layer of the gastric corpus, not the mucosa.
• Capsaicin pretreatment reduced baseline CGRP-li, and subsequent ethanol challenge did not further decrease it, indicating a capsaicin-sensitive source.

Conclusions:

• Concentrated ethanol (≥75%) depletes gastric CGRP-li from a capsaicin-sensitive neuronal pool.
• The muscular layer of the gastric corpus is implicated in this CGRP depletion.
• CGRP may play a protective or modulatory role in the pathogenesis of ethanol-induced gastric hemorrhagic lesions.