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Postconditioning with a volatile anaesthetic in alveolar epithelial cells in vitro

¹ Institute of Anesthesiology, ⁴ Division of Cardiac Anesthesia, Institute of Anesthesiology, and ² Institute of Physiology and Zurich Center for Integrative Human Physiology, University of Zurich, and ³ Dept of Anesthesiology, Orthopedic University Clinic Zurich Balgrist, Zurich, Switzerland.

CORRESPONDENCE: B. Beck-Schimmer, Institute of Anesthesiology, Institute of Physiology and Zurich Center for Integrative Human Physiology, University of Zurich Medical School, Winterthurerstrasse 190, CH-8057 Zurich, Switzerland. Fax: 41 446356814. E-mail: Beatrice_Beck.Schimmer{at}access.uzh.ch

Keywords: Alveolar epithelial cell biology, effector cells, heat shock protein, inflammatory mediators, lung inflammation, nitric oxide

Received: April 15, 2007
Accepted September 10, 2007

Acute lung injury is a common complication in critically ill patients. The present study examined possible immunomodulating effects of the volatile anaesthetic sevoflurane on lipopolysaccharide (LPS)-stimulated alveolar epithelial cells (AEC) in vitro.

Sevoflurane was applied after the onset of injury, simulating a "postconditioning" scenario. Rat AEC were stimulated with LPS for 2 h, followed by a 4-h co-exposure to a CO₂/air mixture with sevoflurane 2.2 volume %; control cells were exposed to the CO₂/air mixture only. Cytokine-induced neutrophil chemoattractant-1, monocyte chemoattractant protein-1, intercellular adhesion molecule-1, as well as the potential protective mediators inducible nitric oxide synthase (iNOS)2 and heat shock protein (HSP)-32, were analysed. Additionally, functional assays (chemotaxis, adherence and cytotoxicity assay) were performed.

A significant reduction of inflammatory mediators in LPS-stimulated, sevoflurane-exposed AEC was found, leading to reduced chemotaxis, neutrophil adherence and neutrophil-induced AEC killing. While iNOS2 was increased in the sevoflurane group, blocking experiments with iNOS2 inhibitor did not affect sevoflurane-induced decrease of inflammatory mediators and AEC killing. Interestingly, sevoflurane treatment also resulted in an enhanced expression of HSP-32.

The data presented in the current study provide strong evidence that anaesthetic postconditioning with sevoflurane mediates cytoprotection in the respiratory compartment in an in vitro model of acute lung injury.