BACKGROUND: Propofol is reported to have protective effects on cerebral ischaemia-induced neuronal death. The aim of this study was to explore whether propofol and halothane can protect hippocampal neuronal function from ischaemic injury during general anaesthesia in rats. METHODS: Rats were divided into 2-vessel occlusion (incomplete cerebral ischaemia) and 4-vessel occlusion (complete cerebral ischaemia) groups consisting of three subgroups each (sham-operated, propofol and halothane groups). One hour after starting propofol 1 mg kg(-1) min(-1) with 30% O2 and N2 or halothane 0.8% in 30% O2 and N2 rats with or without bilateral vertebral artery occlusion had bilateral common carotid arteries occluded by vessel clips for 10 min. Anaesthesia was maintained for another 1 h. Seven days after ischaemia-reperfusion, hippocampal long-term potentiation in the perforant path-dentate gyrus synapse was determined as an index of cerebral outcome. RESULTS: In the propofol groups, the formation of long-term potentiation was significantly impaired in the 2-vessel and 4-vessel occlusion groups compared to the respective sham-operated groups (P < 0.01 and P < 0.05, respectively). Impaired formation of long-term potentiation in propofol groups was comparable to that in halothane groups. The formation of long-team potentiation in the propofol and halothane 2-vessel group was not significantly different from that in the awake 2-vessel group. CONCLUSIONS: Propofol and halothane administered during ischaemia do not possess protective effects against hippocampal neuronal dysfunction induced by cerebral ischaemia-reperfusion as evaluated by our transient ischaemic rat models.
BACKGROUND:Propofol is reported to have protective effects on cerebral ischaemia-induced neuronal death. The aim of this study was to explore whether propofol and halothane can protect hippocampal neuronal function from ischaemic injury during general anaesthesia in rats. METHODS:Rats were divided into 2-vessel occlusion (incomplete cerebral ischaemia) and 4-vessel occlusion (complete cerebral ischaemia) groups consisting of three subgroups each (sham-operated, propofol and halothane groups). One hour after starting propofol 1 mg kg(-1) min(-1) with 30% O2 and N2 or halothane 0.8% in 30% O2 and N2rats with or without bilateral vertebral artery occlusion had bilateral common carotid arteries occluded by vessel clips for 10 min. Anaesthesia was maintained for another 1 h. Seven days after ischaemia-reperfusion, hippocampal long-term potentiation in the perforant path-dentate gyrus synapse was determined as an index of cerebral outcome. RESULTS: In the propofol groups, the formation of long-term potentiation was significantly impaired in the 2-vessel and 4-vessel occlusion groups compared to the respective sham-operated groups (P < 0.01 and P < 0.05, respectively). Impaired formation of long-term potentiation in propofol groups was comparable to that in halothane groups. The formation of long-team potentiation in the propofol and halothane 2-vessel group was not significantly different from that in the awake 2-vessel group. CONCLUSIONS:Propofol and halothane administered during ischaemia do not possess protective effects against hippocampal neuronal dysfunction induced by cerebral ischaemia-reperfusion as evaluated by our transient ischaemic rat models.
Authors: Jie Luo; Su Min; Ke Wei; Jun Cao; Bin Wang; Ping Li; Jun Dong; Yuanyuan Liu Journal: Neuropsychiatr Dis Treat Date: 2014-09-23 Impact factor: 2.570