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Absorption, biotransformation, and storage of halothane.

D A Holaday

    Environmental Health Perspectives
    |December 1, 1977
    PubMed
    Summary

    Halothane biotransformation in humans results in metabolites excreted or irreversibly bound to liver tissues. This process, involving reactive intermediates, can lead to liver damage, especially under anaerobic conditions.

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    Area of Science:

    • Pharmacology
    • Toxicology
    • Biochemistry

    Background:

    • Halothane is a widely used inhalation anesthetic.
    • Understanding its metabolic fate is crucial for patient safety.
    • Previous studies have indicated various metabolic pathways and potential toxic effects.

    Purpose of the Study:

    • To review current knowledge on the quantitative aspects of halothane biotransformation.
    • To elucidate the fate of halothane metabolites in the human body.
    • To assess the relationship between halothane metabolism and potential hepatotoxicity.

    Main Methods:

    • Review of existing literature on halothane metabolism and metabolite analysis.
    • Analysis of urinary metabolite excretion patterns (e.g., trifluoroacetic acid).
    • Examination of plasma bromide ion accumulation and its implications for metabolism duration.

    Main Results:

    • 10-25% of absorbed halothane is recovered as urinary metabolites.
    • Metabolism continues for 20-40 hours post-exposure, with 22-24% metabolized after 8 hours.
    • Trifluoroacetic acid (TFA) is a major urinary metabolite, with excretion confirming biotransformation over 2-3 days.
    • Reactive intermediates and free radical formation are implicated.
    • Irreversible binding of metabolites to liver proteins and lipids occurs, dependent on the P-450 cytochrome system.
    • Hypoxia increases irreversible binding, fluoride release, and hepatic necrosis.

    Conclusions:

    • One-fourth to one-half of halothane undergoes biotransformation in humans.
    • Metabolites are excreted (as TFA, chloride, bromide) or irreversibly bound to hepatic components.
    • Anaerobic conditions exacerbate toxicity, leading to fluoride release, increased binding, and potential liver damage.

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