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Endogenous opioids are not involved in the pathology induced by hyperbaric oxygen treatment

D Jamieson, J Carmody

    Aviation, Space, and Environmental Medicine
    |June 1, 1987
    PubMed

    Insights

    Morphine treatment protects mice from hyperbaric oxygen-induced convulsions and lung damage. This protective effect against high-pressure oxygen toxicity is reversed by naloxone, suggesting an opioid mechanism.

    Area of Science:

    • Pharmacology
    • Toxicology
    • Neuroscience

    Background:

    • Hyperbaric oxygen (5 ATA) causes convulsions and lung damage in mice.
    • Opioid systems are implicated in various physiological responses to stress and drugs.

    Purpose of the Study:

    • To investigate the protective effects of morphine against hyperbaric oxygen toxicity in mice.
    • To explore the role of opioid receptors in mediating this protection.

    Main Methods:

    • Mice were exposed to hyperbaric oxygen (515 kPa; 5 ATA).
    • Morphine (15 mg/kg) or naloxone (1 mg/kg) was administered intraperitoneally.
    • Convulsions and lung pathology (edema, hemorrhage) were assessed.
    • Electric footshock was used as a stressor to induce opioid effects.

    Main Results:

    • Morphine significantly reduced hyperbaric oxygen-induced convulsions and lung damage.
    • Naloxone administration blocked the protective effects of morphine.
    • Electric footshock did not protect against hyperbaric oxygen toxicity.

    Conclusions:

    • Morphine exerts a significant protective effect against hyperbaric oxygen toxicity in mice.
    • The protective mechanism appears to involve opioid receptors, as evidenced by naloxone antagonism.
    • Stress-induced opioid effects do not confer protection against this specific toxicity.

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