Nishino Asuka, Tajima Yosuke, Takuwa Hiroyuki, Masamoto Kazuto, Taniguchi Junko, Wakizaka Hidekatsu, Kokuryo Daisuke, Urushihata Takuya, Aoki Ichio, Kanno Iwao, Tomita Yutaka, Suzuki Norihiro, Ikoma Yoko, Ito Hiroshi
Biophysics Program, Molecular Imaging Center, National Institute of Radiological Sciences, 4-9-1 Anagawa, Chiba 263-8555, Japan.
Department of Neurosurgery, Kimitsu Chuo Hospital, 1010 Sakurai, Kisarazu, Chiba 292-8535, Japan.
Sci Rep. 2016 Apr 27;6:25072. doi: 10.1038/srep25072.
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 [(11)C]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.
我们使用单侧颈总动脉闭塞（UCCAO）的“灌注不良”小鼠模型，研究了脑灌注不足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，结果表明海马体和新皮质没有神经功能缺损。使用激光多普勒血流仪评估对感觉刺激的脑血流（CBF）反应。UCCAO同侧半球对CBF反应的百分比变化在UCCAO前以及UCCAO后7天、14天和28天分别为18.4±3.0%、6.9±2.8%、6.8±2.3%和4.9±2.4%。在UCCAO后7天、14天和28天发现有统计学意义（P<0.01）。与我们之前的研究结果（Tajima等人，2014年）相反，在使用相同模型的UCCAO后28天，对高碳酸血症的CBF反应恢复，而功能性充血在UCCAO后28天持续存在且变得更严重。
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