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Alcohol-chlordiazepoxide interaction

A W Chan, H B Greizerstein, W Strauss

    Pharmacology, Biochemistry, and Behavior
    |July 1, 1982
    PubMed
    Summary
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    Chlordiazepoxide (CDP) and its metabolite NDCDP significantly increase ethanol sleep duration through a supra-additive effect. This potentiation is not due to altered ethanol metabolism but linked to increased CDP and NDCDP levels.

    Area of Science:

    • Pharmacology
    • Neuroscience
    • Toxicology

    Background:

    • Ethanol (alcohol) is known to induce sleep and sedation.
    • Benzodiazepines, such as chlordiazepoxide (CDP), are central nervous system depressants.
    • The interaction between ethanol and benzodiazepines can lead to complex pharmacological effects.

    Purpose of the Study:

    • To investigate the combined effects of chlordiazepoxide (CDP) and its N-demethyl metabolite (NDCDP) on ethanol-induced sleep time in mice.
    • To determine if these effects are related to changes in ethanol elimination rates.
    • To elucidate the role of CDP and NDCDP concentrations in the potentiation of ethanol's sedative effects.

    Main Methods:

    • Mice were administered ethanol alone or in combination with CDP or NDCDP.

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  • Sleep time was measured after ethanol administration.
  • Blood and brain concentrations of ethanol, CDP, and NDCDP were analyzed.
  • Ethanol elimination rates were assessed.

    • Main Results:

    • Both CDP and NDCDP produced a supra-additive increase in ethanol-induced sleep time.
    • These effects were independent of alterations in the rate of blood ethanol elimination.
    • Mice treated with CDP/ethanol exhibited higher blood and brain CDP levels compared to those treated with CDP alone.
    • Comparable increases in sleep time were observed in mice treated with CDP/ethanol or NDCDP/ethanol, with similar NDCDP levels, suggesting NDCDP's significant role.

    Conclusions:

    • Chlordiazepoxide and its metabolite NDCDP potentiate the sedative effects of ethanol in a supra-additive manner.
    • The observed potentiation is primarily attributed to NDCDP and/or its metabolites, rather than altered ethanol metabolism.
    • Increased central nervous system concentrations of CDP and NDCDP likely contribute to the prolonged ethanol-induced sleep time.