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麻醉小鼠大脑皮质扩散性抑制期间脑实质内穿通动脉的动态直径反应及对高碳酸血症血管反应性的消除

Dynamic diameter response of intraparenchymal penetrating arteries during cortical spreading depression and elimination of vasoreactivity to hypercapnia in anesthetized mice.

作者信息

Unekawa Miyuki, Tomita Yutaka, Masamoto Kazuto, Toriumi Haruki, Osada Takashi, Kanno Iwao, Suzuki Norihiro

机构信息

1 Department of Neurology, School of Medicine, Keio University, Tokyo, Japan.

2 Brain Science Inspired Life Support Research Center, University of Electro-Communications, Chofu, Japan.

出版信息

J Cereb Blood Flow Metab. 2017 Feb;37(2):657-670. doi: 10.1177/0271678X16636396. Epub 2016 Jul 21.

Abstract

Cortical spreading depression (CSD) induces marked hyperemia with a transient decrease of regional cerebral blood flow (rCBF), followed by sustained oligemia. To further understand the microcirculatory mechanisms associated with CSD, we examined the temporal changes of diameter of intraparenchymal penetrating arteries during CSD. In urethane-anesthetized mice, the diameter of single penetrating arteries at three depths was measured using two-photon microscopy during passage of repeated CSD, with continuous recordings of direct current potential and rCBF. The first CSD elicited marked constriction superimposed on the upstrokes of profound dilation throughout each depth of the penetrating artery, and the vasoreaction temporally corresponded to the change of rCBF. Second or later CSD elicited marked dilation with little or no constriction phase throughout each depth, and the vasodilation also temporally corresponded to the increase of rCBF. Furthermore, the peak dilation showed good negative correlations with basal diameter and increase of rCBF. Vasodilation induced by 5% CO inhalation was significantly suppressed after CSD passage at any depth as well as hyperperfusion. These results may indicate that CSD-induced rCBF changes mainly reflect the diametric changes of the intraparenchymal arteries, despite the elimination of responsiveness to hypercapnia.

摘要

皮层扩散性抑制(CSD)会引发显著的充血,同时局部脑血流量(rCBF)短暂下降,随后出现持续性缺血。为了进一步了解与CSD相关的微循环机制,我们研究了CSD期间脑实质内穿通动脉直径的时间变化。在氨基甲酸乙酯麻醉的小鼠中,在重复CSD通过期间,使用双光子显微镜测量三个深度处单个穿通动脉的直径,并连续记录直流电位和rCBF。首次CSD在穿通动脉各深度的深度扩张上升期引发显著收缩,血管反应在时间上与rCBF的变化相对应。第二次或之后的CSD在各深度引发显著扩张,几乎没有或没有收缩期,血管舒张在时间上也与rCBF的增加相对应。此外,峰值扩张与基础直径和rCBF的增加呈良好的负相关。在任何深度通过CSD后,5%二氧化碳吸入诱导的血管舒张以及高灌注均受到显著抑制。这些结果可能表明,尽管对高碳酸血症的反应性消失,但CSD诱导的rCBF变化主要反映了脑实质内动脉的直径变化。

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