Long-term effects of cerebral hypoperfusion on neural density and function using misery perfusion animal model.
Long-term effects of cerebral hypoperfusion on neural density and function using misery perfusion animal model.
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DOI：
10.1038/srep25072
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发表时间：
2016-04-27
影响因子：
4.6
通讯作者：
Ito H
中科院分区：
文献类型：
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作者：
Nishino A;Tajima Y;Takuwa H;Masamoto K;Taniguchi J;Wakizaka H;Kokuryo D;Urushihata T;Aoki I;Kanno I;Tomita Y;Suzuki N;Ikoma Y;Ito H
本研究采用单侧颈总动脉闭塞（UCCAO）的痛苦灌流小鼠模型，研究了脑低灌注对神经元密度和功能性充血的慢性影响。在UCCAO后28天，使用[11 C]氟马西尼-PET和组织学评估神经元密度，表明海马和新皮质无神经功能缺损。使用激光多普勒血流仪评估CBF对感觉刺激的反应。缺血前、缺血后7、14和28天，同侧大脑半球CBF反应性变化百分比分别为18.4 ± 3.0%、6.9 ± 2.8%、6.8 ± 2.3%和4.9 ± 2.4%。术后7、14、28天与对照组比较差异有统计学意义（P < 0.01）。与我们先前的发现（Tajima等人，2014）相反，使用相同模型在UCCAO后28天恢复了CBF对高碳酸血症的反应，功能性充血持续存在，并在UCCAO后28天恶化。
We investigated the chronic effects of cerebral hypoperfusion on neuronal density and functional hyperemia using our misery perfusion mouse model under unilateral common carotid artery occlusion (UCCAO). Neuronal density evaluated 28 days after UCCAO using [11C]flumazenil-PET and histology indicated no neurologic deficit in the hippocampus and neocortex. CBF response to sensory stimulation was assessed using laser-Doppler flowmetry. Percentage changes in CBF response of the ipsilateral hemisphere to UCCAO were 18.4 ± 3.0%, 6.9 ± 2.8%, 6.8 ± 2.3% and 4.9 ± 2.4% before, and 7, 14 and 28 days after UCCAO, respectively. Statistical significance was found at 7, 14 and 28 days after UCCAO (P < 0.01). Contrary to our previous finding (Tajima et al. 2014) showing recovered CBF response to hypercapnia on 28 days after UCCAO using the same model, functional hyperemia was sustained and became worse 28 days after UCCAO.