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Hepatocellular membrane function during chronic burn injury.

J P Minei1, Y Fong, M A Marano

  • 1Department of Surgery, New York Hospital- Cornell Medical Center, New York 10021.

The Journal of Surgical Research
|April 1, 1989
PubMed
Summary
This summary is machine-generated.

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Hepatocellular membrane dysfunction, indicated by depolarization, occurs after injury. This study shows burn and infection in rats leads to hepatic membrane hyperpolarization, maintaining liver function during critical illness.

Area of Science:

  • Physiology
  • Hepatology
  • Burn Medicine

Background:

  • Hepatocellular membrane dysfunction (depolarization) is linked to acute injury and bacteremia.
  • The role of hepatocellular membrane potential during combined thermal injury and infection is not well understood.

Purpose of the Study:

  • To investigate hepatocellular membrane potential changes in rats with concurrent burn injury and Pseudomonas aeruginosa infection.
  • To determine if hepatic membrane dysfunction occurs in the setting of ongoing thermal injury and infection.

Main Methods:

  • Wistar rats were subjected to sham burn, burn, or burn with infection (Pseudomonas aeruginosa).
  • Hepatocellular transmembrane potentials, body and liver weights, and hepatic ATP, RNA, DNA, and protein contents were measured on days 3 and 7 post-injury.

Related Experiment Videos

  • Corticosterone levels were also assessed.
  • Main Results:

    • By day 7, burn/infected rats showed conserved hepatic mass despite significant weight loss.
    • Hepatic transmembrane potential hyperpolarized significantly in burn/infected rats compared to controls.
    • Burn/infected rats exhibited increased hepatic RNA and DNA content, with elevated corticosterone levels.

    Conclusions:

    • Hepatic membrane hyperpolarization and increased RNA content were observed in rats with combined burn and infection.
    • These changes were specific to the combined insult and not solely due to burn or starvation.
    • Hepatic membrane hyperpolarization may be a mechanism for maintaining liver function during severe burn infections.