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Department of Anesthesiology and Critical Care Medicine, Kagoshima University School of Medicine, Kagoshima, Japan
Address correspondence and reprint requests to Yoshitami Kadota, MD, Department of Anesthesiology and Critical Care Medicine, Kagoshima University School of Medicine, Sakuragaoka 8-35-1, Kagoshima, 890-8520, Japan. Address e-mail to kadotayo{at}med4.kufm.kagoshima-u.ac.jp
Using precision-cut liver slices (2025 mg wet weight) from male Wistar rats, we examined whether clinically relevant propofol concentrations have hepatoprotective or -toxic effects during hypoxia/reoxygenation. Slices were preincubated for 2 h in sealed roller vials (three slices per vial) containing Waymouths medium (37°C; 95% oxygen/5% CO2). Then, propofol or Intralipid was added to create four different groups (control, Intralipid, small-concentration propofol [0.51.5 µg/mL], and large-concentration propofol [2.06.0 µg/mL]). Thereafter, each group was incubated for 4 h under 95% oxygen/5% CO2 (no hypoxia) or for 2 h under 100% nitrogen plus 2 h under 95% oxygen/5% CO2 (hypoxia/reoxygenation). Slice viability and hypoxia/reoxygenation injury were assessed at 2, 3, and 4 h after incubation began by using the slice intracellular K+ concentration, energy status (adenosine triphosphate content, total adenine nucleotides content, and energy charge), and liver enzyme leakage (aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase). Propofol and Intralipid caused a significant delay in energy charge recovery in comparison with the control. There were no significant differences between the propofol groups and the other two groups in intracellular K+ content or liver enzyme leakage. Propofol had no hepatotoxic effect under no-hypoxia conditions in rat liver slices, nor did it have a protective effect against hypoxia/reoxygenation-induced hepatic injury.
IMPLICATIONS: Propofol had no hepatotoxic effect under no-hypoxia conditions in rat liver slices, nor did it have a protective effect against hypoxia/reoxygenation-induced hepatic injury.
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