Isoflurane inhalation after induction of endotoxemia in rats attenuates the systemic cytokine response.

BACKGROUND/AIMS: Volatile anesthetics are frequently utilized in clinical routine. Isoflurane has been shown to attenuate the response to inflammatory stimuli such as lipopolysaccharide (LPS) when administered before induction of endotoxemia. We aimed therefore to evaluate the effect of isoflurane after administration of LPS on the cytokine release as a therapeutic option.

MATERIALS AND METHODS: 21 male Sprague-Dawley rats were randomly assigned to the following groups: animals that received LPS (5 mg/kg, i.v.) without further intervention (LPS group), animals that received continuous inhalation of 1 minimum alveolar concentration (MAC) isoflurane 15 min after administration of LPS (Iso group) and no specific intervention (sham group). Four hours following LPS injection, plasma levels of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), IL-6 and IL-10 were determined. Furthermore, nitrite release from cultured alveolar macrophages was analyzed.

RESULTS: Inhalation of isoflurane after induction of endotoxemia attenuated the release of TNF-alpha (-52%, p < 0.05) and IL-1 beta (-39%, p < 0.05) as compared to the LPS group, while IL-6 and IL-10 levels were not significantly altered. Nitrite release was significantly increased in the Iso group as compared to the LPS group (+115%, p < 0.05).

CONCLUSION: Inhalation of 1 MAC isoflurane after induction of endotoxemia in rats attenuates the systemic release of proinflammatory cytokines and concurrently enhances the production of nitrite in cultured alveolar macrophages.