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首页> 外文期刊>European journal of anaesthesiology >Effects of propofol and halothane on long-term potentiation in the rat hippocampus after transient cerebral ischaemia.
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Effects of propofol and halothane on long-term potentiation in the rat hippocampus after transient cerebral ischaemia.

机译:异丙酚和氟烷对短暂性脑缺血后大鼠海马长时程增强的影响。

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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.
机译:背景:据报道,异丙酚对脑缺血引起的神经元死亡具有保护作用。这项研究的目的是探讨丙泊酚和氟烷是否可以在大鼠全麻期间保护海马神经元免受缺血性损伤。方法:将大鼠分为两支血管阻塞(不完全性脑缺血)和四支血管阻塞(完全性脑缺血)组,每组由三个亚组(假手术组,异丙酚和氟烷组)组成。异丙酚1 mg kg(-1)min(-1)与30%O2和N2大鼠中有30%O2和N2或氟烷的0.8%开始使用后,有或没有双侧椎动脉闭塞的一小时后,双侧颈总动脉被血管夹阻塞10分钟麻醉再维持1小时。缺血-再灌注后7天,将穿孔路径齿状回突触中的海马长期增强作用确定为大脑预后的指标。结果:与假手术组相比,丙泊酚组的2血管阻塞组和4血管阻塞组的长期增强作用明显减弱(分别为P <0.01和P <0.05)。丙泊酚组的长期增强作用减弱与氟烷组相似。异丙酚和氟烷2容器组的长队增强的形成与清醒2容器组的形成没有显着差异。结论:根据我们的短暂性缺血大鼠模型评估,缺血期间给予的异丙酚和氟烷对脑缺血再灌注所致的海马神经元功能障碍没有保护作用。

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