Persisting depletion of brain glucose following cortical spreading depression, despite apparent hyperaemia: evidence for risk of an adverse effect of Leao's spreading depression

Persisting depletion of brain glucose following cortical spreading depression, despite apparent hyperaemia: evidence for risk of an adverse effect of Leao's spreading depression
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DOI:
10.1038/jcbfm.2008.108
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发表时间:
2009-01-01
影响因子:
6.3
通讯作者:
Boutelle, Martyn G.
Boutelle, Martyn G.
中科院分区:
医学1区
文献类型:
--
作者:
Hashemi, Parastoo;Bhatia, Robin;Boutelle, Martyn G.

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快速取样微透析(rsMD)直接对大脑皮层允许识别葡萄糖和乳酸的组合时间序列签名,其特征在于在实验性局灶性缺血中的梗死周围去极化,但没有可比的数据存在与正常灌注的大脑中的充血相关的“经典”皮质扩散性抑制(CSD)。在这里,我们研究了透析液葡萄糖和乳酸盐的rsMD反应五个高血扩散性抑郁症引起的皮质内微量注射,通常为1 mol/L氯化钾,在开颅准备在5只猫氯醛糖麻醉。用微电极验证去极化,并使用激光散斑流量计来检查MD探针附近的事件和灌注响应的传播。去极化后10分钟,透析液葡萄糖下降28%,乳酸升高58%。去极化后30分钟透析液葡萄糖未恢复。平均基线指示性脑血流量为25.5 +/- 4.1 mL/100 g/min,平均最大充血增加为29.6 +/- 6 mL/100 g/min; CSD后30分钟仍存在充血。由于CSD事件在人类急性脑损伤中是重复的、频繁的并且通常在时间上聚集,因此这些结果表明与先前被认为在很大程度上是良性的模式的去极化事件相关的细胞外葡萄糖消耗的高风险。
Rapid sampling microdialysis (rsMD) directed towards the cerebral cortex has allowed identification of a combined time-series signature for glucose and lactate that characterizes peri-infarct depolarization in experimental focal ischaemia, but no comparable data exist for 'classical' cortical spreading depression (CSD) associated with hyperaemia in the normally perfused brain. Here, we examined the rsMD responses of dialysate glucose and lactate to five hyperaemic spreading depressions induced with intracortical microinjections, typically of 1 mol/L KCI, in open-skull preparations in five cats under chloralose anaesthesia. Depolarization was verified with microelectrodes, and laser speckle flowmetry was used to examine propagation of the events and perfusion responses near the MD probe. Ten minutes after depolarization, dialysate glucose fell and lactate rose by 28% and 58% respectively. There was no recovery of dialysate glucose 30 mins after depolarization. Mean baseline indicative cerebral blood flow was 25.5 +/- 4.1 mL/100 g/min and mean maximum hyperaemic increase was by 29.6 +/- 6 mL/100 g/min; hyperaemia remained present 30 mins after CSD. As CSD events are repetitive, frequent, and often clustered temporally in human acute brain injury, these results indicate a high risk of depletion of extracellular glucose in association with depolarization events of a pattern previously thought to be largely benign.