INTRODUCTION: Sevoflurane is well known to exert a neuroprotective effect through anesthetic preconditioning. However, its effects on postconditioning, a neuroprotective phenomenon following an insult, have not been well studied. AIMS: In this study, we examined the ability of sevoflurane to induce postconditioning in rat hippocampal slices, in vitro. RESULTS: 2%, 4%, and 6% sevoflurane reduced neurophysiologic and morphologic neuronal injury following oxygen-glucose deprivation (OGD) and reperfusion. The quantity of damaged neurons was significantly reduced on immunofluorescence staining; excitatory amino acids (Asp, Glu) increased and inhibitory amino acids (GABA) decreased significantly. The effect was concentration-dependent. CONCLUSION: Postconditioning with sevoflurane reduces neuronal damage after OGD-reperfusion injury in the CA1 area of rat hippocampus, in vitro.
INTRODUCTION:Sevoflurane is well known to exert a neuroprotective effect through anesthetic preconditioning. However, its effects on postconditioning, a neuroprotective phenomenon following an insult, have not been well studied. AIMS: In this study, we examined the ability of sevoflurane to induce postconditioning in rat hippocampal slices, in vitro. RESULTS: 2%, 4%, and 6% sevoflurane reduced neurophysiologic and morphologic neuronal injury following oxygen-glucose deprivation (OGD) and reperfusion. The quantity of damaged neurons was significantly reduced on immunofluorescence staining; excitatory amino acids (Asp, Glu) increased and inhibitory amino acids (GABA) decreased significantly. The effect was concentration-dependent. CONCLUSION: Postconditioning with sevoflurane reduces neuronal damage after OGD-reperfusion injury in the CA1 area of rat hippocampus, in vitro.