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Morphine metabolites

L L Christrup1

  • 1Department of Pharmaceutics, Royal Danish School of Pharmacy, Copenhagen, Denmark.

Acta Anaesthesiologica Scandinavica
|January 1, 1997
PubMed
Summary
This summary is machine-generated.

Morphine metabolites morphine-6-glucuronide (M6G) and morphine-3-glucuronide (M3G) contribute to analgesia and side effects. M6G is a potent analgesic, while M3G may cause hyperalgesia and influence tolerance.

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Area of Science:

  • Pharmacology
  • Neuroscience
  • Medicinal Chemistry

Background:

  • Morphine is a primary opioid analgesic with poor lipid solubility.
  • Major metabolites morphine-3-glucuronide (M3G) and morphine-6-glucuronide (M6G) are formed in the liver, brain, and kidneys.
  • These glucuronides are primarily eliminated via bile and urine.

Purpose of the Study:

  • To investigate the pharmacological roles of morphine metabolites M3G and M6G.
  • To understand their contribution to morphine's analgesic effects and side effects.
  • To explore their penetration into the brain and interaction with opioid receptors.

Main Methods:

  • Analysis of M3G and M6G concentrations in cerebrospinal fluid (CSF) and plasma.
  • Assessment of analgesic and other effects after central administration in rats (ICV, IT).

Related Experiment Videos

  • Utilizing high-performance liquid chromatography (HPLC) for quantitative determination of morphine and its metabolites.

    • Main Results:

    • M6G exhibits significant analgesic properties, with potency up to 800 times greater than morphine in rats.
    • M3G does not bind to opioid receptors but can antagonize analgesia and ventilatory depression.
    • M3G may cause non-opioid mediated hyperalgesia, allodynia, and convulsions, potentially explaining side effects of high-dose morphine.

    Conclusions:

    • M6G significantly contributes to morphine's analgesia.
    • M3G may play a role in morphine tolerance and is associated with adverse effects like hyperalgesia and convulsions.
    • Despite polarity, morphine glucuronides can cross the blood-brain barrier, influencing central effects.