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Effect of sevoflurane on human neutrophil apoptosis

Published online by Cambridge University Press:  02 June 2005

R. Tyther ,
J. O'Brien ,
J. Wang ,
H. P. Redmond  and
G. Shorten
R. Tyther
Affiliation:
Cork University Hospital, Department of Anaesthesia and Intensive Care Medicine, Cork, Ireland
J. O'Brien
Affiliation:
Cork University Hospital, Department of Anaesthesia and Intensive Care Medicine, Cork, Ireland
J. Wang
Affiliation:
Cork University Hospital, Department of Surgery, Cork, and University College Cork, Cork, Ireland
H. P. Redmond
Affiliation:
Cork University Hospital, Department of Surgery, Cork, and University College Cork, Cork, Ireland
G. Shorten
Affiliation:
Cork University Hospital, Department of Anaesthesia and Intensive Care Medicine, Cork, Ireland
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Abstract

Summary

Background and objective: Both chronic occupational exposure to volatile anaesthetic agents and acute in vitro exposure of neutrophils to isoflurane have been shown to inhibit the rate of apoptosis of human neutrophils. It is possible that inhibition of neutrophil apoptosis arises through delaying mitochondrial membrane potential collapse. We assessed mitochondrial depolarization and apoptosis in unexposed neutrophils and neutrophils exposed to sevoflurane in vivo.

Methods: A total of 20 mL venous blood was withdrawn pre- and postinduction of anaesthesia, the neutrophils isolated and maintained in culture. At 1, 12 and 24 h in culture, the percentage of neutrophil apoptosis was assessed by dual staining with annexin V-FITC and propidium iodide. Mitochondrial depolarization was measured using the dual emission styryl dye JC-1.

Results: Apoptosis was significantly inhibited in neutrophils exposed to sevoflurane in vivo at 24 (exposed: 38 (12)% versus control: 28 (11)%, P = 0.001), but not at 1 or 12 h, in culture. Mitochondrial depolarization was not delayed in neutrophils exposed to sevoflurane.

Conclusions: The most important findings are that sevoflurane inhibits neutrophil apoptosis in vivo and that inhibition is not mediated primarily by an effect on mitochondrial depolarization.

Keywords

ANAESTHESIA GENERAL, anaesthesia, inhalation, sevofluraneBLOOD CELLS, leukocytes, granulocytes, neutrophilsCELL DEATH, apoptosisPATHOLOGICAL PROCESSES, inflammation
Type
Original Article
Information
European Journal of Anaesthesiology , Volume 20 , Issue 2 , February 2003 , pp. 111 - 115
Copyright
2003 European Society of Anaesthesiology

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References

Wyllie AH, Kerr JFR, Currie AR. Cell death: the significance of apoptosis. Int Rev Cytol 1980; 68: 251–230.Google Scholar
Duvall E, Wyllie AH. Macrophage recognition of cells undergoing programmed cell death (apoptosis). Immunology 1985; 56: 35–38.Google Scholar
Cohen JJ. Programmed cell death in the immune system. Adv Immunol 1991; 50: 55–85.Google Scholar
Tyther R, Halligan M, Wang J, Redmond HP, Shorten G. The effects of isoflurane at clinical concentrations in vitro on neutrophil apoptosis? Ir J Med Sci 2001; 170: 41–44.Google Scholar
Zaugg M, Jamali NZ, Lucchinetti E, Shafiq SA, Siddiqui MA. Norepinephrine-induced apoptosis is inhibited in adult rat ventricular myocytes exposed to volatile anesthetics. Anesthesiology 2000; 93: 209–218.Google Scholar
Savill J. Apoptosis in resolution of inflammation. J Leukoc Biol 1997; 61: 375–380.Google Scholar
Petit PX, Susin SA, Zamzani N, Mignotte B, Kroemer G. Mitochondria and programmed cell death: back to the future. FEBS Lett 1996; 396: 7–13.Google Scholar
Carmody RJ, Cotter TG. Molecular events and mechanisms of apoptosis. Sepsis 1998; 2: 9–19.Google Scholar
Kam PC, Ferch NI. Apoptosis: mechanisms and clinical implications. Anaesthesia 2000; 55: 1081–1093.Google Scholar
Green DR, Reed JC. Mitochondria and apoptosis. Science 1998; 281: 1309–1312.Google Scholar
Zamzami N, Susin SA, Marchetti P, et al. Mitochondrial control of nuclear apoptosis. J Exp Med 1996; 183: 1533–1544.Google Scholar
Vander Heiden MG, Chandel NS, Williamson EK, Schumacker PT, Thompson CB. Bcl-xL regulates the membrane potential and volume homeostasis of mito-chondria. Cell 1997; 91: 627–637.Google Scholar
Zamzami N, Marchetti P, Castedo M, et al. Inhibitors of permeability transition interfere with the disruption of the mitochondrial transmembrane potential during apoptosis. FEBS Lett 1996; 384: 53–57.Google Scholar
Ward C, Wong TH, Murray J, et al. Induction of human neutrophil apoptosis by nitric oxide donors: evidence for a caspase-dependent, cyclic-GMP-independent, mechanism. Biochem Pharmacol 2000; 59: 305–314.Google Scholar
Shimizu S, Eguchi Y, Kamiike W. Bcl-2 prevents apoptotic mitochondrial dysfunction by regulating proton flux. Proc Natl Acad Sci USA 1998; 95: 1455–1459.Google Scholar
Thornberry NA, Lazebnik Y. Caspases: enemies within. Science 1998; 281: 1312–1316.Google Scholar
Haslett C. Granulocyte apoptosis and its role in the resolution of lung inflammation. Am J Resp Crit Care Med 1999; 160: S5–S11.Google Scholar