Effects of propofol on early phase of warm hepatic ischemia/reperfusion injury

Hepatogastroenterology. 2007 Dec;54(80):2333-6.

Abstract

Background/aims: It is still unclear whether propofol may protect the liver against ischemia/ reperfusion injury (IRI) in vivo.

Methodology: The livers of male Sprague-Dawley rats were subjected to 60 minutes of partial normothermic ischemia allowing perfusion to right and caudate lobes and subsequent 45 minutes of reperfusion. Either propofol (Propofol group, n = 11, 10 mg/ kg/h) or saline (Control group, n = 11) was continuously administered. At the end of reperfusion blood and liver samples were taken to analyze malondialdehyde, hepatic injury score, palmitate oxidation rate, serum AST and ALT concentrations.

Results: The malondialdehyde concentration (micromol/g tissue, mean +/- SD) was decreased in the Propofol group (1.39 +/- 0.21, perfused lobes and 1.85 +/- 0.27, ischemic reperfused lobes) compared with Control group (1.97 +/- 0.20, perfused lobes and 2.39 +/- 0.28, ischemic reperfused lobes) (P < 0.01). Hepatic injury scores were decreased in Propofol group compared with Control group (P < 0.01), but with mild hepatic injury in both groups. There were no differences of serum AST and ALT concentrations, and palmitate oxidation rate between groups.

Conclusions: Propofol might be effective mainly in attenuation of lipid peroxidation with only minimal hepatocellular protection during the early phase of warm hepatic IRI in vivo.

MeSH terms

  • Alanine Transaminase / blood
  • Animals
  • Aspartate Aminotransferases / blood
  • Lipid Peroxidation / drug effects
  • Liver / blood supply*
  • Male
  • Malondialdehyde / analysis
  • Palmitic Acid / metabolism
  • Propofol / therapeutic use*
  • Rats
  • Rats, Sprague-Dawley
  • Reperfusion Injury / metabolism
  • Reperfusion Injury / prevention & control*

Substances

  • Palmitic Acid
  • Malondialdehyde
  • Aspartate Aminotransferases
  • Alanine Transaminase
  • Propofol