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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.

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。

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