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Increased glucose availability does not restore prolonged spreading depression durations in hypotensive rats without brain injury.葡萄糖供应增加并不能恢复无脑损伤低血压大鼠延长的扩散性抑制持续时间。
Exp Neurol. 2012 Dec;238(2):130-2. doi: 10.1016/j.expneurol.2012.08.013. Epub 2012 Aug 19.
2
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Perfusion pressure-dependent recovery of cortical spreading depression is independent of tissue oxygenation over a wide physiologic range.在广泛的生理范围内,皮质扩散性抑制的灌注压力依赖性恢复与组织氧合无关。
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The acute effects of hemorrhagic shock on cerebral blood flow, brain tissue oxygen tension, and spreading depolarization following penetrating ballistic-like brain injury.穿透性弹道样脑损伤后失血性休克对脑血流、脑组织氧张力和扩散性去极化的急性影响。
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Increased 20-HETE synthesis explains reduced cerebral blood flow but not impaired neurovascular coupling after cortical spreading depression in rat cerebral cortex.皮质扩散性抑制后大鼠大脑皮层 20-HETE 合成增加解释脑血流减少,但不能解释神经血管耦联受损。
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本文引用的文献

1
K⁺ dynamics in ischemic rat brain in vivo by ⁸⁷Rb MRI at 7 T.7T 下 ⁸⁷Rb MRI 活体观察缺血性大鼠脑内 K⁺ 动力学。
NMR Biomed. 2011 Aug;24(7):778-83. doi: 10.1002/nbm.1652. Epub 2011 Jan 25.
2
Perfusion pressure-dependent recovery of cortical spreading depression is independent of tissue oxygenation over a wide physiologic range.在广泛的生理范围内,皮质扩散性抑制的灌注压力依赖性恢复与组织氧合无关。
J Cereb Blood Flow Metab. 2010 Jun;30(6):1168-77. doi: 10.1038/jcbfm.2009.285. Epub 2010 Jan 20.
3
Persisting depletion of brain glucose following cortical spreading depression, despite apparent hyperaemia: evidence for risk of an adverse effect of Leão's spreading depression.尽管出现明显充血,但皮质扩散性抑制后大脑葡萄糖持续耗竭:关于莱昂扩散性抑制产生不良影响风险的证据
J Cereb Blood Flow Metab. 2009 Jan;29(1):166-75. doi: 10.1038/jcbfm.2008.108. Epub 2008 Sep 24.
4
Hypoxia and hypotension transform the blood flow response to cortical spreading depression from hyperemia into hypoperfusion in the rat.缺氧和低血压会使大鼠大脑皮质扩散性抑制的血流反应从充血转变为灌注不足。
J Cereb Blood Flow Metab. 2008 Jul;28(7):1369-76. doi: 10.1038/jcbfm.2008.35. Epub 2008 Apr 30.
5
The management of plasma glucose in acute cerebral ischaemia and traumatic brain injury: more research needed.急性脑缺血和创伤性脑损伤中血糖的管理:仍需更多研究。
Intensive Care Med. 2008 Jul;34(7):1169-72. doi: 10.1007/s00134-008-1045-4. Epub 2008 Mar 5.
6
Directed sampling for electrolyte analysis and water content of micro-punch samples shows large differences between normal and ischemic rat brain cortex.针对微冲压样品的电解质分析和水分含量进行的定向采样显示,正常大鼠脑皮质和缺血大鼠脑皮质之间存在巨大差异。
Brain Res. 2000 Jun 23;868(2):370-5. doi: 10.1016/s0006-8993(00)02360-x.
7
Excessive oxygen or glucose supply does not alter the blood flow response to somatosensory stimulation or spreading depression in rats.过量的氧气或葡萄糖供应不会改变大鼠对体感刺激或扩散性抑制的血流反应。
Brain Res. 1997 Jul 4;761(2):290-9. doi: 10.1016/s0006-8993(97)00354-5.
8
Influence of plasma glucose concentration on rat brain extracellular calcium transients during spreading depression.扩散性抑制期间血浆葡萄糖浓度对大鼠脑细胞外钙瞬变的影响。
J Cereb Blood Flow Metab. 1993 Jan;13(1):179-82. doi: 10.1038/jcbfm.1993.21.
9
Transport of potassium at the blood-brain barrier.血脑屏障处钾的转运
J Physiol. 1972 Mar;221(3):617-32. doi: 10.1113/jphysiol.1972.sp009771.
10
Regional changes in tissue pH and glucose content during cortical spreading depression in rat brain.大鼠脑皮层扩散性抑制期间组织pH值和葡萄糖含量的区域变化。
Brain Res. 1985 Jun 10;336(1):167-70. doi: 10.1016/0006-8993(85)90430-5.

葡萄糖供应增加并不能恢复无脑损伤低血压大鼠延长的扩散性抑制持续时间。

Increased glucose availability does not restore prolonged spreading depression durations in hypotensive rats without brain injury.

机构信息

Neurovascular Research Laboratory, Department of Radiology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.

出版信息

Exp Neurol. 2012 Dec;238(2):130-2. doi: 10.1016/j.expneurol.2012.08.013. Epub 2012 Aug 19.

DOI:10.1016/j.expneurol.2012.08.013
PMID:22981452
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3498578/
Abstract

Maintenance of transmembrane ionic gradients and their restoration after cortical spreading depression (CSD) are energy dependent. We recently showed an inverse relationship between blood pressure and CSD duration that is independent of tissue oxygenation. Here, we tested the alternative hypothesis that glucose availability becomes rate-limiting for CSD recovery upon reduced blood pressure in anesthetized rats under full systemic physiological monitoring. Hypotension induced by controlled exsanguination significantly prolonged CSD durations, reduced propagation speeds, and diminished the blood flow response. Hyperglycemia failed to restore the prolonged CSD durations in hypotensive rats and did not significantly alter the propagation speed or the blood flow response. These data suggest that prolonged CSD durations during reduced cerebral perfusion pressure are independent of tissue energy status, and implicate alternative mechanisms of CSD recovery such as vascular clearance of extracellular K(+).

摘要

维持跨膜离子梯度及其在皮质扩散性抑制(CSD)后的恢复依赖于能量。我们最近发现,血压与 CSD 持续时间之间存在反比关系,且这种关系与组织氧合无关。在这里,我们在全身生理监测下,通过麻醉大鼠进行实验,检验了在血压降低时,葡萄糖供应是否会成为 CSD 恢复的限速因素这一替代假说。通过控制性放血引起的低血压显著延长了 CSD 持续时间,降低了传播速度,并减少了血流反应。在低血压大鼠中,高血糖未能恢复延长的 CSD 持续时间,也没有显著改变传播速度或血流反应。这些数据表明,在脑灌注压降低期间,CSD 持续时间延长与组织能量状态无关,并暗示了 CSD 恢复的替代机制,如细胞外 K(+)的血管清除。