Research article summary (published 30 Oct 2009):

Isoflurane preconditioning ameliorates endotoxin-induced acute lung injury and mortality in rats.

Full Abstract

BACKGROUND: The effects of isoflurane pretreatment on pulmonary proinflammatory cytokines and survival in severe endotoxin-induced acute lung injury (ALI) have not been studied systemically. We investigated the effect of preadministration of isoflurane on ALI induced by lipopolysaccharide (LPS) in rats. METHODS: Male Sprague-Dawley rats weighing 250-300 g were randomly assigned to 1 of 4 groups: sham rats (injected intraperitoneally [IP] with saline) pretreated with vehicle (100% O(2)) (sham-vehicle); sham rats pretreated with isoflurane (sham-ISO); LPS rats (injected IP with LPS) pretreated with vehicle (vehicle-LPS); and LPS rats pretreated with isoflurane (ISO-LPS). Endotoxemia was induced by IP injection of LPS. Isoflurane 1.4% was administered 30 min before LPS injection. The animals were then observed for 6 h. We monitored arterial blood pressure, heart rate, and blood gas. The extent of ALI was evaluated by lung wet/dry ratio, Evans blue dye extravasation, and histologic examination. We also measured pulmonary nitric oxide (NO), tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6 levels. In addition, survival statistics and pulmonary inducible NO synthase (iNOS) gene expression were also determined. RESULTS: LPS caused systemic hypotension and severe ALI, as evidenced by the increases in the extent of ALI, impairment of pulmonary functions, and increases in pulmonary NO, TNF-alpha, IL-1beta, and IL-6. Isoflurane preconditioning mitigated systemic hypotension and the development of ALI. Isoflurane preconditioning also attenuated the LPS-induced increases in pulmonary nitrate/nitrite and proinflammatory cytokine release and improved survival of rats with severe sepsis. The expression of iNOS was upregulated by LPS and reduced by isoflurane pretreatment. CONCLUSIONS: Isoflurane preconditioning can attenuate pulmonary proinflammatory cytokine release and decrease the mortality induced by severe sepsis. Early protection seems to be mediated partly through inhibition of iNOS-NO pathway activation.

Author information

Author/s: Li, Qi Fang (QF); Zhu, Ye Sen (YS); Jiang, Hong (H); Xu, Hui (H); Sun, Yu (Y);

Affiliation: Department of Anesthesiology, Shanghai Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Journal and publication information

Publication Type: Journal Article; Research Support, Non-U.S. Gov't

Journal: Anesthesia and analgesia (Anesth Analg), published in United States. (Language: eng)

Reference: 2009-Nov; vol 109 (issue 5) : pp 1591-7

Dates: Created 2009/10/21; Completed 2009/11/05;

PMID: 19843795, status: MEDLINE (last retrieval date: 11/5/2009, IMS Date: )

Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.

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MeSH headings (categories)

This article was linked to the MESH Headings shown below.

Acid-Base Equilibrium - drug effects Acute Lung Injury - chemically induced; metabolism; pathology; physiopathology; prevention & control Animals Cytoprotection Disease Models, Animal Endotoxemia - chemically induced; drug therapy; metabolism; pathology; physiopathology Hemodynamics - drug effects Hypotension - chemically induced; prevention & control Interleukin-1beta - metabolism Interleukin-6 - metabolism Isoflurane - pharmacology

Lipopolysaccharides Lung - drug effects; metabolism; pathology; physiopathology Male Nitric Oxide - metabolism Nitric Oxide Synthase Type II - metabolism Oxygen - blood Protective Agents - pharmacology Rats Rats, Sprague-Dawley Time Factors Tumor Necrosis Factor-alpha - metabolism

Associated Chemicals: Interleukin-1beta (0) ; Interleukin-6 (0) ; Lipopolysaccharides (0) ; Protective Agents (0) ; Tumor Necrosis Factor-alpha (0) ; lipopolysaccharide, Escherichia coli 0111 B4 (0) ; Nitric Oxide (10102-43-9) ; Isoflurane (26675-46-7) ; Oxygen (7782-44-7) ; Nitric Oxide Synthase Type II (EC 1.14.13.39) ; Nos2 protein, rat (EC 1.14.13.39)

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