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Endogenous opiates and stress ulceration

J E Morley, A S Levine, S E Silvis

    Life Sciences
    |August 16, 1982
    PubMed
    Summary

    Naltrexone, an opiate antagonist, protects against stress ulcers by blocking peripheral opiates. This cytoprotective effect is independent of central opiate actions on stomach acid secretion.

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    Area of Science:

    • Gastroenterology
    • Pharmacology
    • Physiology

    Background:

    • Stress-induced ulceration is a significant clinical concern.
    • Endogenous opiates and their antagonists play a role in gastrointestinal physiology.
    • The precise mechanisms of opiate involvement in stress ulceration are not fully understood.

    Purpose of the Study:

    • To investigate the cytoprotective effect of naltrexone against stress-induced gastric ulceration.
    • To determine whether the effect of naltrexone is mediated by central or peripheral opiate receptors.
    • To explore the relationship between opiate actions, gastric acid secretion, and mucosal blood flow in the context of stress ulceration.

    Main Methods:

    • Parenteral administration of naltrexone in a model of stress-induced ulceration.
    • Assessment of cytoprotective effects.
    • Evaluation of the role of central versus peripheral opiate receptor blockade.

    Main Results:

    • Parenteral naltrexone demonstrated a significant cytoprotective effect against stress-induced ulcers.
    • The protective effect was attributed to the blockade of peripheral endogenous opiates.
    • The mechanism was independent of central opiate inhibition of gastric acid secretion.

    Conclusions:

    • Naltrexone exhibits cytoprotective properties against stress ulcers via peripheral opiate antagonism.
    • Peripheral opiate pathways are implicated in the pathogenesis of stress-induced gastric mucosal damage.
    • Opiate modulation of gastric mucosal blood flow may be a key factor in stress ulceration.

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