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在大鼠海马区匹罗卡品诱导的癫痫持续状态活动期间,脑血流发生变化。

Cerebral blood flow changes during pilocarpine-induced status epilepticus activity in the rat hippocampus.

机构信息

Radiology and Physics Unit, UCL Institute of Child Health, University College London, London, UK.

出版信息

Exp Neurol. 2010 Sep;225(1):196-201. doi: 10.1016/j.expneurol.2010.06.015. Epub 2010 Jun 25.

DOI:10.1016/j.expneurol.2010.06.015
PMID:20599541
Abstract

INTRODUCTION

There is a known relationship between convulsive status epilepticus (SE) and hippocampal injury. Although the precise causes of this hippocampal vulnerability remains uncertain, potential mechanisms include excitotoxicity and ischaemia. It has been hypothesised that during the early phase of seizures, cerebral blood flow (CBF) increases in the cortex to meet energy demand, but it is unclear whether these compensatory mechanisms occur in the hippocampus. In this study we investigated CBF changes using perfusion MRI during SE in the pilocarpine rat.

METHODS

First, we determined whether SE could be induced under anaesthesia. Two anaesthetic protocols were investigated: isoflurane (n=6) and fentanyl/medetomidine (n=7). Intrahippocampal EEG electrodes were used to determine seizure activity and reflex behaviours were used to assess anaesthesia. Pilocarpine was administered to induce status epilepticus. For CBF measurements, MRI arterial spin labelling was performed continuously for up to 3h. Either pilocarpine (375 mg/kg) (n=7) for induction of SE or saline (n=6) was administered. Diazepam (10mg/kg) was administered i.p. 90 min after the onset of SE.

RESULTS AND DISCUSSION

We demonstrated time-dependent significant (p<0.05) differences between the CBF responses in the parietal cortex and the hippocampus during SE. This regional response indicates a preferential distribution of flow to certain regions of the brain and may contribute to the selective vulnerability observed in the hippocampus in humans.

摘要

简介

癫痫持续状态(SE)与海马损伤之间存在已知关系。尽管这种海马易损性的确切原因尚不清楚,但潜在的机制包括兴奋性毒性和缺血。有人假设,在癫痫发作的早期阶段,大脑皮质的脑血流(CBF)增加以满足能量需求,但尚不清楚这些代偿机制是否发生在海马体中。在这项研究中,我们使用匹鲁卡品大鼠的灌注 MRI 研究了 SE 期间的 CBF 变化。

方法

首先,我们确定了 SE 是否可以在麻醉下诱导。研究了两种麻醉方案:异氟烷(n=6)和芬太尼/右美托咪定(n=7)。海马内 EEG 电极用于确定癫痫发作活动,反射行为用于评估麻醉。给予匹鲁卡品诱导 SE。进行 MRI 动脉自旋标记以连续测量长达 3 小时的 CBF。用匹鲁卡品(375mg/kg)(n=7)诱导 SE 或生理盐水(n=6)进行 CBF 测量。SE 发作后 90 分钟,腹腔内给予地西泮(10mg/kg)。

结果和讨论

我们证明了 SE 期间大脑皮质和海马体之间的 CBF 反应存在时间依赖性显著差异(p<0.05)。这种区域反应表明血流优先分布到大脑的某些区域,这可能有助于解释人类海马体中观察到的选择性易损性。

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