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British Journal of Anaesthesia, 2001, Vol. 86, No. 4 550-554
© 2001 The Board of Management and Trustees of the British Journal of Anaesthesia

Effects of sevoflurane on dopamine, glutamate and aspartate release in an in vitro model of cerebral ischaemia

C. C. Toner1, K. Connelly2, R. Whelpton2, S. Bains2, A. T. Michael-Titus2, D. P. McLaughlin1 and J. A. Stamford1

1Neurotransmission Laboratory, Academic Department of Anaesthesia and Intensive Care, The Royal London and St Bartholomew’s School of Medicine and Dentistry, Royal London Hospital, Whitechapel, London E1 1BB, UK. 2Division of Biomedical Sciences, Queen Mary & Westfield College, Mile End Road, London E1 4NS, UK*Corresponding author

Release of excitatory amino acids and dopamine plays a central role in neuronal damage after cerebral ischaemia. In the present study, we used an in vitro model of ischaemia to investigate the effects of sevoflurane on dopamine, glutamate and aspartate efflux from rat corticostriatal slices. Slices were superfused with artificial cerebrospinal fluid at 34°C and episodes of ‘ischaemia’ were mimicked by removal of oxygen and reduction in glucose concentration from 4 to 2 mmol litre–1 for <=30 min. Dopamine efflux was monitored in situ by voltammetry while glutamate and aspartate concentrations in samples of the superfusate were measured by HPLC with fluorescence detection. Neurotransmitter outflow from slices was measured in the absence or presence of sevoflurane (4%). After induction of ischaemia in control slices, there was a mean (SEM) delay of 166 (7) s (n=5) before sudden efflux of dopamine which reached a maximum extracellular concentration of 77.0 (15.2) µmol litre–1. Sevoflurane (4%) reduced the rate of dopamine efflux during ischaemia (6.90 (1.5) and 4.73 (1.76) µmol litre–1 s–1 in controls and sevoflurane-treated slices, respectively; P<0.05), without affecting its onset or magnitude. Excitatory amino acid efflux was much slower. Ischaemia-induced glutamate efflux had not reached maximum after 30 min of ischaemia. Basal (pre-ischaemic) glutamate and aspartate efflux per slice was 94.8 (24.8) and 69.3 (31.5) nmol litre–1 superfusate (n=4) and was not significantly reduced by 4% sevoflurane. Ischaemia greatly increased glutamate and aspartate efflux (to a maximum of 919 (244)% and 974 (489)% of control, respectively). However, ischaemia-induced efflux of both glutamate and aspartate was significantly reduced by 4% sevoflurane (P<0.001 for glutamate, P<0.01 for aspartate). In summary, sevoflurane may owe part of its reported neuroprotective effect to a reduction of ischaemia-induced efflux of excitatory amino acids and, to a lesser extent, dopamine.

Br J Anaesth 2001; 86: 550–4


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