@article{oai:repo.qst.go.jp:00047760,
 author = {Nishino, Asuka and Tajima, Yosuke and Takuwa, Hiroyuki and Masamoto, Kazuto and Taniguchi, Junko and Wakizaka, Hidekatsu and Kokuryo, Daisuke and Urushihata, Takuya and Aoki, Ichio and Kanno, Iwao and Tomita, Yutaka and Suzuki, Norihiro and Ikoma, Yoko and Ito, Hiroshi and 西野 明日香 and 田桑 弘之 and 脇坂 秀克 and 漆畑 拓弥 and 青木 伊知男 and 生駒 洋子 and 伊藤 浩},
 journal = {Scientific Reports},
 month = {Apr},
 note = {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.},
 pages = {25072-1--25072-8},
 title = {Long-term effects of cerebral hypoperfusion on neural density and function using misery perfusion animal model.},
 volume = {6},
 year = {2016}
}