Substantial Reduction of Parenchymal Cerebral Blood Flow in Mice with Bilateral Common Carotid Artery Stenosis.

Substantial Reduction of Parenchymal Cerebral Blood Flow in Mice with Bilateral Common Carotid Artery Stenosis.
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DOI:
10.1038/srep32179
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发表时间:
2016-08-18
期刊:
影响因子:
4.6
通讯作者:
Ihara M
Ihara M
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Hattori Y;Enmi J;Iguchi S;Saito S;Yamamoto Y;Nagatsuka K;Iida H;Ihara M

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双侧颈总动脉狭窄(BCAS)小鼠模型复制了慢性脑灌注不足和白质缺血性病变,被认为可以模拟血管性认知障碍的某些方面。激光散斑流量计已证实 BCAS 后脑表面的脑血流量 (CBF) 变化,但脑实质中的 CBF 水平仍然未知。使用外部微线圈对成年 C57BL/6J 雄性小鼠进行 BCAS。进行脑磁共振血管造影(MRA)以可视化颅内主动脉,同时使用动脉自旋标记(ASL)来测量 BCAS 前后的皮质和皮质下实质 CBF 水平。脑 MRA 显示前循环流量大幅减少,直到 BCAS 后 14 天,在接下来的 14 天逐渐但不完全恢复,大脑后动脉的侧支循环可能生长。 ASL 显示,在 BCAS 后 1 天和 14 天期间,皮质和皮质下实质 CBF 仍下降约基线水平的 50%,在第 28 天恢复至约 70%。在 BCAS 模型中,实质中的 CBF 水平低于 BCAS 模型中的皮质浅层区域,并且在 BCAS 后的前 2 周内保持下降状态而没有恢复。这些结果表明 BCAS 模型可靠地复制了慢性脑灌注不足。
The bilateral common carotid artery stenosis (BCAS) mouse model, which replicates chronic cerebral hypoperfusion and white matter ischemic lesions, is considered to model some aspects of vascular cognitive impairment. Cerebral blood flow (CBF) changes in the brain surface post-BCAS have been demonstrated by laser speckle flowmetry, but CBF levels in the brain parenchyma remain unknown. Adult C57BL/6J male mice were subjected to BCAS using external microcoils. Brain magnetic resonance angiography (MRA) was conducted to visualize the intracranial main arteries while arterial spin labeling (ASL) was used to measure cortical and subcortical parenchymal CBF levels before and after BCAS. Brain MRA showed anterior circulation flow was substantially decreased until 14 days post-BCAS, which gradually but incompletely recovered over the following 14 days, with probable growth of collaterals from the posterior cerebral artery. ASL showed that cortical and subcortical parenchymal CBF remained decreased at approximately 50% of the baseline level during 1 and 14 days post-BCAS, recovering to approximately 70% at day 28. CBF levels in the parenchyma were lower than the cortical superficial region in the BCAS model and remained decreased without recovery during the first 2 weeks post-BCAS. These results suggest that the BCAS model reliably replicates chronic cerebral hypoperfusion.