Hepatocellular membrane function during chronic burn injury

Joseph P. Minei, Yuman Fong, Michael A. Marano, Lyle L. Moldawer, William G. Jones, He Wei, Richard P. Richardson, Roger W. Yurt, G. Tom Shires, Stephen F. Lowry, G. Tom Shires

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


Hepatocellular membrane dysfunction, as indicated by depolarization of the membrane potential, occurs after acute injury and early bacteremia. To determine whether hepatocellular membrane dysfunction occurs in the setting of ongoing thermal injury and infection, Wistar rats were divided into four groups: (1) sham-burned, freely fed controls (FF); (2) rats sustaining ≈30% total body surface area dorsal full-thickness scald burn (Burn); (3) rats sustaining burns as in group 2 followed by immediate inoculation of 1 × 108 CFU Pseudomonas aeruginosa (Burn/Inf); and (4) sham-burned rats pair-fed to the food intake of the Burn/Inf group (PF). On the third and seventh days postburn, body and liver weights were determined. In vivo hepatocellular transmembrane potentials were measured and hepatic ATP, RNA, DNA, and protein contents were assayed. By Day 7, despite greater weight loss in the Burn/Inf group than due to starvation alone (P < 0.01 Burn/Inf vs FF and PF), hepatic mass was conserved. This was associated with hyperpolarization of the hepatic transmembrane potential (-46.6 ± 1.5 vs -32.1 ± 0.6 mV, Burn/Inf vs FF, P < 0.01) and increases in RNA (141 ± 9 vs 91 ± 4 mg/liver, Burn/Inf vs FF, P < 0.01) and DNA (37 ± 5 vs 22 ± 2 mg/liver, Burn/Inf vs FF, P < 0.05) contents, with no change in ATP or hepatic protein contents. There was a significant hypercorticosteronemia observed in the Burn/Inf group (43 ± 9 vs 2.8 ± 0.7 μg/dl, Burn/Inf vs FF, P < 0.01). This hepatic membrane hyperpolarization and augmented RNA content were not secondary to burn or starvation alone as the response in these groups was significantly less than that of the Burn/Inf group. It is suggested that this hepatic membrane hyperpolarization is one mechanism by which hepatic function is maintained during ongoing burn infection in the rat.

Original languageEnglish (US)
Pages (from-to)311-316
Number of pages6
JournalJournal of Surgical Research
Issue number4
StatePublished - Apr 1989

ASJC Scopus subject areas

  • Surgery


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