Effect of different concentrations of sevoflurane pretreatment on acute lung injury induced by endotoxin in rats

Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2010 Sep;35(9):921-7. doi: 10.3969/j.issn.1672-7347.2010.09.004.

Abstract

Objective: To investigate the effect of 3 concentrations of sevoflurane pretreatment on acute lung injury induced by endotoxin in rats.

Methods: Thirty-six male SD rats were randomly divided into 6 groups:a control group(Group A), a sevoflurane group(Group B), a 3.6% sevoflurane pretreatment group(Group C), a 2.4% Sevoflurane pretreatment group(Group D), a 1.2% sevo sevoflurane pretreatment group(Group E), and lipopolysaccharide (Group F).The rats were killed 6 h after lipopolysaccharide (LPS) or saline injection.Histological examinations of the lung tissues were performed with light microscope. Lung wet/dry weight (W/D) ratio, myeloperoxidase (MPO) activity, and intercellular adhesion molecule-1 (ICAM-1) mRNA expression were assayed.

Results: Introvenous LPS significantly aggravated lung tissue damage,increased lung W/D ratio, MPO activity, and lung ICAM-1 mRNA expression compared with the control group(P<0.05). Precondition with 2.4% sevoflurane significantly attenuated the above-mentioned changes induced by LPS (P<0.05). The 3.6% LPS (Group C) significantly attenuated lung tissue damage and decreased MPO activity,lung ICAM-1 mRNA expression compared with the Group F (P<0.05),but no significant change in lung W/D ratio was seen (P>0.05). MPO activity was significantly decreased in Group E (P<0.05), but lung W/D ratio and lung ICAM-1 mRNA expression had no significant changes (P>0.05).

Conclusion: Precondition with 2.4% sevoflurane can reduce LPS-induced lung injury in rats. Decreased expression of ICAM-1 and less accumulation of neutrophils were participated in its mechanism.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Acute Lung Injury / chemically induced
  • Acute Lung Injury / metabolism
  • Acute Lung Injury / prevention & control*
  • Anesthetics, Inhalation
  • Animals
  • Dose-Response Relationship, Drug
  • Intercellular Adhesion Molecule-1 / genetics
  • Intercellular Adhesion Molecule-1 / metabolism
  • Lipopolysaccharides*
  • Male
  • Methyl Ethers / pharmacology
  • Methyl Ethers / therapeutic use*
  • Protective Agents / pharmacology
  • Protective Agents / therapeutic use
  • RNA, Messenger / genetics
  • RNA, Messenger / metabolism
  • Random Allocation
  • Rats
  • Rats, Sprague-Dawley
  • Sevoflurane

Substances

  • Anesthetics, Inhalation
  • Lipopolysaccharides
  • Methyl Ethers
  • Protective Agents
  • RNA, Messenger
  • Intercellular Adhesion Molecule-1
  • Sevoflurane