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BJA Advance Access originally published online on October 14, 2005
British Journal of Anaesthesia 2005 95(6):803-810; doi:10.1093/bja/aei256
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© The Board of Management and Trustees of the British Journal of Anaesthesia 2005. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Effects of ketamine and propofol on inflammatory responses of primary glial cell cultures stimulated with lipopolysaccharide

Y. Saito Shibakawa1, Y. Sasaki2, Y. Goshima2, N. Echigo1, Y. Kamiya1, K. Kurahashi1, Y. Yamada1 and T. Andoh1,*

Departments of 1 Anesthesiology and Critical Care Medicine and 2 Molecular Pharmacology and Neurobiology, Yokohama City University Graduate School of Medicine, 3–9 Fukuura, Kanazawa-ku, Yokohama 236-0004, Japan

* Corresponding author. Present address: Department of Anesthesiology, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Yamanashi 409-3898, Japan. E-mail: tando{at}yamanashi.ac.jp

Background. Ketamine has been reported to exert anti-inflammatory effects on macrophages stimulated with lipopolysaccharide (LPS) in vitro and in vivo. Several studies have reported conflicting results regarding the effects of propofol on cytokine production from immune cells. However, there have been no reports of the effects of these agents on inflammatory responses in glial cells. We investigated the effects of ketamine and propofol on LPS-induced production of nitric oxide, tumour necrosis factor-{alpha} (TNF-{alpha}) and prostaglandin E2 (PGE2) from primary cultures of rat glial cells in vitro.

Methods. Glial cells were stimulated with LPS in the absence and presence of various concentrations of ketamine (30–1000 µM) or propofol (30 and 300 µM). Nitric oxide released into the culture media was determined by measuring nitrite using the Griess reaction, and concentrations of TNF-{alpha} and PGE2 were measured by enzyme-linked immunosorbent assay (ELISA).

Results. Ketamine reduced LPS-induced TNF-{alpha} production without significant inhibition of nitrite release in mixed glial cells, astrocyte cultures and microglial cultures. Ketamine also inhibited LPS-induced production of PGE2 in astrocyte cultures. In contrast, propofol had no effect on LPS-induced nitrite or TNF-{alpha} production in mixed glial cells.

Conclusions. The data demonstrate that ketamine inhibited some of the inflammatory responses of both astrocytes and microglial cells treated with LPS without causing major change in nitric oxide release. Propofol had no effect on the production of nitric oxide or TNF-{alpha} from LPS-stimulated glial cells.


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