The involvement of endotoxin in halothane-associated liver injury

R. C. Lind, A. J. Gandolfi, I. G. Sipes, B. R. Brown

Research output: Contribution to journalArticlepeer-review

23 Scopus citations


Since endotoxin, lipopolysaccharides (LPS), have been implicated as a causative factor in the development of hepatic necrosis in rats exposed to hepatotoxic levels of several chemical agents, the role of LPS in the halothane-hypoxia (HH) model of hepatic damage in male Sprague-Dawley rats was investigated. When injected intravenously immediately after halothane anesthesia, a subnecrotic dose of LPS (0.5 mg/kg; Escherichia coli 026:B6) was found to markedly potentiate HH-induced hepatic necrosis. Pretreatment of the animals with the antiendotoxin agent, lactulose, prior to exposure to halothane reduced the hepatic damage normally seen from HH. A possible mechanism of LPS-induced potentiation was indicated by changes in hepatic calcium levels at 24 h after treatment. Endogenous LPS may play a role in HH-induced hepatic necrosis, and the mechanism of LPS-induced potentiation may be due to an LPS-related membrane dysfunction.

Original languageEnglish (US)
Pages (from-to)544-550
Number of pages7
Issue number5
StatePublished - 1984

ASJC Scopus subject areas

  • Anesthesiology and Pain Medicine


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