Preventive effects of sevoflurane treatment on lung inflammation in rats

Asian Pac J Trop Med. 2013 Jan;6(1):53-6. doi: 10.1016/S1995-7645(12)60200-4.

Abstract

Objective: To observe the effects of sevoflurane treatment on lung inflammation in rats with lipopoIysaccharide-induced acute lung injury (ALI).

Methods: The rat model of ALI was established by intratracheal instillation of lipopolysaccharide (LPS). 45 infantile SD rats [body weight (272±15) g] were randomly divided into 3 groups (n=15): control group, LPS group, sevoflurane group. NS (1 mL/kg) was instillated in rats' airways of control group; LPS (5 mg/kg) was instillated in rats' airways of LPS group. Sevoflurane group rats received sevoflurane (2.4%) inhalation for a hour after LPS was instillated in rats' airways. Six hours after NS or LPS instillation, all rats were exsanguinated. Lung tissues were examined by HE staining. Expressions of TNF-α and ICAM1 mRNA were detected by semiquantitative RT-PCR techniques. The protein level of TNF-α and ICAM1 were assessed by western blot techniques.

Results: In LPS group the permeability of lung tissues increased, organizational structure severely damaged and the alveolar wall tumed thick, with interstitial edema and Europhiles infiltrated increasingly. The LPS group had higher mRNA expressions of TNF-α and ICAM1 than control group and sevoflurane group (P<0.05), and LPS group had higher protein level of TNF-α and ICAM1 than control group and sevoflurane group (P<0.05).

Conclusions: Sevoflurane treatment can attenuate lung inflammation in rats with lipopolysaccharide-induced acute lung injury.

MeSH terms

  • Acute Lung Injury / chemically induced
  • Acute Lung Injury / metabolism
  • Acute Lung Injury / pathology
  • Administration, Inhalation
  • Animals
  • Gene Expression / drug effects
  • Gene Expression / immunology
  • Intercellular Adhesion Molecule-1 / genetics
  • Intercellular Adhesion Molecule-1 / metabolism
  • Lipopolysaccharides / administration & dosage
  • Lung / chemistry
  • Lung / metabolism
  • Lung / pathology
  • Male
  • Methyl Ethers / pharmacology*
  • Pneumonia / drug therapy
  • Pneumonia / metabolism
  • Pneumonia / pathology
  • Pneumonia / prevention & control*
  • Protective Agents / administration & dosage
  • Protective Agents / pharmacology*
  • Random Allocation
  • Rats
  • Rats, Sprague-Dawley
  • Sevoflurane
  • Tumor Necrosis Factor-alpha / genetics
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Lipopolysaccharides
  • Methyl Ethers
  • Protective Agents
  • Tumor Necrosis Factor-alpha
  • Intercellular Adhesion Molecule-1
  • Sevoflurane