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Anesth Analg 2008; 106:830-837
© 2008 International Anesthesia Research Society
doi: 10.1213/ane.0b013e3181616fc9
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ANESTHETIC PHARMACOLOGY

Hepatic Energy Metabolism and the Differential Protective Effects of Sevoflurane and Isoflurane Anesthesia in a Rat Hepatic Ischemia-Reperfusion Injury Model

Nurdan Bedirli, MD*, Ebru Ofluoglu, PhD{dagger}, Mustafa Kerem, MD{ddagger}, Gulten Utebey, MD*, Murat Alper, MD§, Demet Yilmazer, MD§, Abdulkadir Bedirli, MD{ddagger}, Onur Ozlu, MD*, and Hatice Pasaoglu, MD{dagger}

From the *Department of Anesthesiology, Diskapi Training and Research Hospital; Departments of {dagger}Biochemistry and {ddagger}General Surgery, Gazi University Medical School; and §Department of Pathology, Diskapi Training and Research Hospital, Ankara, Turkey.

Address correspondence and reprint requests to Nurdan Bedirli, MD, Mesa Koru Sit. Fulya Blok, 85/39, 06810, Cayyolu, Ankara, Turkey. Address e-mail to nurbedirli{at}yahoo.com.

BACKGROUND: We investigated the effects of isoflurane and sevoflurane in a warm liver ischemia-reperfusion (IR) model on cytokines, hepatic tissue blood flow (HTBF), energy content, and liver structure.

METHODS: Seventy-two Wistar rats were randomly assigned into 1 of 3 groups: Control group, no volatile anesthetics; sevoflurane group, 2% sevoflurane; isoflurane group, 1.5% isoflurane. Thirty minutes after the start of volatile anesthetics, rats were subjected to 45 min hepatic ischemia and 2 and 4 h of reperfusion. Rats were killed at the end of ischemia, 2 and 4 h of reperfusion. Aspartate aminotransferase and alanine aminotransferase, HTBF, malondialdehyde, tumor necrosis factor (TNF)-{alpha}, interleukin (IL)-1β, energy charge, and histologic examination were used to evaluate the extent of liver injury.

RESULTS: Serum alanine aminotransferase and aspartate aminotransferase levels were similar in control and isoflurane groups while there was a significant decrease in the sevoflurane group in the postischemic period (P < 0.01). HTBF was remarkably better in the sevoflurane group than in the isoflurane group and worse in the control group. Tissue malondialdehyde levels were significantly low in the sevoflurane group compared with the isoflurane group at 2 h of reperfusion (P < 0.05) and reached its maximum value in the postischemic period in the control group. After ischemia, 2 and 4 h of reperfusion, tumor necrosis factor-{alpha} and interleukin-1β values were lowest in the sevoflurane group and highest in the control group but it was not statistically significant (P > 0.05). In the sevoflurane group, hepatic adenosine triphosphate and energy charge were significantly high at all measurement times. At the postischemic period, energy charge was lower compared with the sevoflurane and isoflurane groups. The degree of hepatocyte injury was small in the sevoflurane group.

CONCLUSIONS: Clinically relevant concentrations of sevoflurane given before, during, and after hepatic ischemia protected the liver against IR injury, whereas the effects of isoflurane on hepatic IR injury were not notable.







Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press
Copyright © 2008 by the International Anesthesia Research Society.