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Hepatocyte dysfunction in thermal injury.

G T Shires, S A Albert, H Illner

    The Journal of Trauma
    |October 1, 1983
    PubMed
    Summary
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    Burn shock causes severe cellular dysfunction, indicated by decreased liver cell transmembrane potential difference (PD). This dysfunction is not due to energy depletion but likely ion transport failure, partially reversed by resuscitation.

    Area of Science:

    • Physiology
    • Cell Biology
    • Biochemistry

    Background:

    • Transmembrane potential difference (PD) reflects cellular function.
    • Hemorrhagic shock and burn shock can lead to cellular dysfunction.
    • Previous studies suggested energy depletion as a cause of decreased PD.

    Purpose of the Study:

    • To correlate changes in liver and muscle PD with hepatocyte ATP, glucose-6-phosphate (G-6-P), and lactate levels during burn shock and resuscitation.
    • To investigate the mechanism of cellular dysfunction in burn shock.

    Main Methods:

    • Six baboons underwent severe scald burns (52.4% BSA).
    • Muscle and liver PD were monitored.
    • Hepatocyte ATP, G-6-P, and lactate levels were measured during burn shock and resuscitation.

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  • Resuscitation followed the Parkland formula.

    • Main Results:

    • Liver PD significantly decreased in burn shock (46.2 to 22.4 mV) and partially recovered with resuscitation.
    • Hepatocyte ATP and G-6-P levels remained stable.
    • Lactate levels increased threefold during burn shock.
    • Muscle PD fell to -70 mV before resuscitation.

    Conclusions:

    • Severe hepatocyte depolarization occurs in burn shock, indicating cellular derangement.
    • Stable intracellular ATP levels exclude energy depletion as the cause of dysfunction.
    • Cellular dysfunction in burn shock may result from impaired ion transport or altered membrane permeability.
    • Fluid resuscitation partially restores cellular function.