BACKGROUND AND OBJECTIVE: We sought to test whether a transient myocardial ischaemia can induce impairment of hippocampal long-term potentiation (LTP) and whether sevoflurane preconditioning can provide robust protective effects on this neurological impairment. METHODS: Wistar rats were subjected to a transient coronary artery occlusion for 30 min. Sevoflurane preconditioning was performed by exposure to 1.0 minimum alveolar concentration of sevoflurane for 1 h and washout for 30 min before myocardial ischaemia. Hippocampal LTP was evaluated during a 7-day observation period. The expressions of haem oxygenase-1 mRNA, tumour necrosis factor-alpha mRNA and interleukin-1beta mRNA in the hippocampus were analysed by quantitative reverse transcription-PCR. RESULTS: LTP was significantly inhibited 1 and 3 days after the transient myocardial ischaemia in the control group when compared with the animals subjected to a sham operation without coronary occlusion, and the LTP recovered to a normal magnitude 7 days later. Sevoflurane preconditioning remarkably reversed the transient inhibition of LTP observed at 1 and 3 days after myocardial ischaemia. Compared with the sham animals, the expressions of haem oxygenase-1 mRNA, tumour necrosis factor-alpha mRNA and interleukin-1beta mRNA in the hippocampus of the control rats were significantly increased during the early stage after myocardial ischaemia (1-3 days), and the increases of these cytokines were attenuated by sevoflurane pretreatment. CONCLUSION: Sevoflurane preconditioning induced neuroprotection against impairment of hippocampal LTP resulting from myocardial ischaemia and reperfusion.
BACKGROUND AND OBJECTIVE: We sought to test whether a transient myocardial ischaemia can induce impairment of hippocampal long-term potentiation (LTP) and whether sevoflurane preconditioning can provide robust protective effects on this neurological impairment. METHODS:Wistar rats were subjected to a transient coronary artery occlusion for 30 min. Sevoflurane preconditioning was performed by exposure to 1.0 minimum alveolar concentration of sevoflurane for 1 h and washout for 30 min before myocardial ischaemia. Hippocampal LTP was evaluated during a 7-day observation period. The expressions of haem oxygenase-1 mRNA, tumour necrosis factor-alpha mRNA and interleukin-1beta mRNA in the hippocampus were analysed by quantitative reverse transcription-PCR. RESULTS: LTP was significantly inhibited 1 and 3 days after the transient myocardial ischaemia in the control group when compared with the animals subjected to a sham operation without coronary occlusion, and the LTP recovered to a normal magnitude 7 days later. Sevoflurane preconditioning remarkably reversed the transient inhibition of LTP observed at 1 and 3 days after myocardial ischaemia. Compared with the sham animals, the expressions of haem oxygenase-1 mRNA, tumour necrosis factor-alpha mRNA and interleukin-1beta mRNA in the hippocampus of the control rats were significantly increased during the early stage after myocardial ischaemia (1-3 days), and the increases of these cytokines were attenuated by sevoflurane pretreatment. CONCLUSION:Sevoflurane preconditioning induced neuroprotection against impairment of hippocampal LTP resulting from myocardial ischaemia and reperfusion.