BACKGROUND AND OBJECTIVE: Commonly used anaesthetics can cause neurodegeneration in the developing brain. Sevoflurane, a widely used substance in paediatric anaesthesia, has not been analysed thus far. This study was carried out to investigate the effects of sevoflurane on neuronal cell viability. METHODS: Primary cortical neuronal cultures were prepared from Wistar rat embryos (E18), kept in 100 microl Gibco-Neurobasal-A medium and exposed to 4 and 8 Vol.% sevoflurane for up to 48 h. Cell viability was assessed using the methyltetrazolium assay and was related to untreated controls. To evaluate the role of gamma-aminobutyric acid type A receptors, untreated cells were preincubated with the receptor antagonists gabazine or picrotoxin and were subsequently exposed to 8 Vol.% sevoflurane and the receptor antagonist. Cell viability was assessed and compared with that of sevoflurane-treated controls. RESULTS: Up to 6 (8 Vol.%) and 12 h (4 Vol.%) of exposure to sevoflurane, cell viability was equal when compared with untreated controls. Only longer exposure times led to significantly lowered cell viability. After 12 h of exposure, no significant differences in cell viability were found between these two series. Cell viability of cultures treated with sevoflurane and the receptor antagonists showed no significant differences when compared with sevoflurane-exposed controls. CONCLUSION: These results suggest that sevoflurane does not cause neurodegeneration in primary cortical neurons of the rat following clinically relevant exposure times and concentrations.
BACKGROUND AND OBJECTIVE: Commonly used anaesthetics can cause neurodegeneration in the developing brain. Sevoflurane, a widely used substance in paediatric anaesthesia, has not been analysed thus far. This study was carried out to investigate the effects of sevoflurane on neuronal cell viability. METHODS: Primary cortical neuronal cultures were prepared from Wistar rat embryos (E18), kept in 100 microl Gibco-Neurobasal-A medium and exposed to 4 and 8 Vol.% sevoflurane for up to 48 h. Cell viability was assessed using the methyltetrazolium assay and was related to untreated controls. To evaluate the role of gamma-aminobutyric acid type A receptors, untreated cells were preincubated with the receptor antagonists gabazine or picrotoxin and were subsequently exposed to 8 Vol.% sevoflurane and the receptor antagonist. Cell viability was assessed and compared with that of sevoflurane-treated controls. RESULTS: Up to 6 (8 Vol.%) and 12 h (4 Vol.%) of exposure to sevoflurane, cell viability was equal when compared with untreated controls. Only longer exposure times led to significantly lowered cell viability. After 12 h of exposure, no significant differences in cell viability were found between these two series. Cell viability of cultures treated with sevoflurane and the receptor antagonists showed no significant differences when compared with sevoflurane-exposed controls. CONCLUSION: These results suggest that sevoflurane does not cause neurodegeneration in primary cortical neurons of the rat following clinically relevant exposure times and concentrations.