Sevoflurane ameliorates gas exchange and attenuates lung damage in experimental lipopolysaccharide-induced lung injury.
BACKGROUND
Acute lung injury is a common complication in critically ill patients. Several studies suggest that volatile anesthetics have immunomodulating effects. The aim of the current study was to assess possible postconditioning with sevoflurane in an in vivo model of endotoxin-induced lung injury.


METHODS
Rats were anesthetized, tracheotomized, and mechanically ventilated. Lipopolysaccharide (saline as control) was administered intratracheally. Upon injury after 2 h of propofol anesthesia, general anesthesia was continued with either sevoflurane or propofol for 4 h. Arterial blood gases were measured every 2 h. After 6 h of injury, bronchoalveolar lavage was performed and lungs were collected. Total cell count, albumin content, concentrations of the cytokines cytokine-induced neutrophil chemoattractant-1 and monocyte chemoattractant protein-1, and phospholipids were analyzed in bronchoalveolar lavage fluid. Expression of messenger RNA for the two cytokines and for surfactant protein B was determined in lung tissue. Histopathologic examination of the lung was performed.


RESULTS
Significant improvement of the ratio of oxygen tension to inspired oxygen fraction was shown with sevoflurane (mean + or - SD: 243 + or - 94 mmHg [32.4 kPa]) compared with propofol (88 + or - 19 mmHg [11.7 kPa]). Total cell count representing effector cell recruitment as well as albumin content as a measure of lung permeability were significantly decreased in the sevoflurane-lipopolysaccharide group compared with the propofol-lipopolysaccharide group in bronchoalveolar lavage fluid. Expression of the cytokines protein in bronchoalveolar lavage fluid as well as messenger RNA in lung tissue was significantly lower in the sevoflurane-lipopolysaccharide group compared with the propofol-lipopolysaccharide group.


CONCLUSIONS
Postconditioning with sevoflurane attenuates lung damage and preserves lung function in an in vivo model of acute lung injury.
Voigtsberger
Stefanie
S
Institute of Anesthesiology, University of Zurich, Zurich, Switzerland.
Lachmann
Robert A
RA
Leutert
Anik C
AC
Schläpfer
Martin
M
Booy
Christa
C
Reyes
Livia
L
Urner
Martin
M
Schild
Julia
J
Schimmer
Ralph C
RC
Beck-Schimmer
Beatrice
B
D018685:Anesthetics, Inhalation / Q000633:toxicity*; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D002452:Cell Count; D002478:Cells, Cultured; D018932:Chemokine CCL2 / Q000096:biosynthesis / Q000235:genetics; D054360:Chemokine CXCL1 / Q000096:biosynthesis / Q000235:genetics; D018925:Chemokines / Q000378:metabolism; D042783:Endothelial Cells; D004797:Enzyme-Linked Immunosorbent Assay; D006935:Hypercapnia / Q000378:metabolism; D008070:Lipopolysaccharides; D008171:Lung Diseases / Q000139:chemically induced* / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D008738:Methyl Ethers / Q000633:toxicity*; D010539:Permeability; D010743:Phospholipids / Q000032:analysis; D015742:Propofol / Q000494:pharmacology; D011651:Pulmonary Artery / Q000166:cytology / Q000187:drug effects; D011659:Pulmonary Gas Exchange / Q000502:physiology*; D011663:Pulmonary Surfactants / Q000032:analysis / Q000302:isolation & purification; D012313:RNA / Q000096:biosynthesis / Q000302:isolation & purification; D051381:Rats; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D000077149:Sevoflurane
D018685:Anesthetics, Inhalation; C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; D054360:Chemokine CXCL1; D018925:Chemokines; C513297:Cxcl1 protein, rat; D008070:Lipopolysaccharides; D008738:Methyl Ethers; D010743:Phospholipids; D011663:Pulmonary Surfactants; D000077149:Sevoflurane; D012313:RNA; D015742:Propofol