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脳血管障害と虚血 1
Cerebrovascular Disease and Ischemia 1

開催日 2014/9/13
時間 17:10 - 18:10
会場 Room I(311+312)
Chairperson(s) 八木田 佳樹 / Yoshiki Yagita (川崎医科大学脳卒中医学教室 / Department of Stroke Medicine, Kawasaki Medical School, Japan)
山内 浩 / Hiroshi Yamauchi (滋賀県立成人病センター研究所 / Shiga Medical Center Research Institute, Japan)

A Novel Rat Model of Subcortical Ischemic Vascular Dementia with Ameroid Constrictor

  • O3-I-5-3
  • 北村 彰浩 / Akihiro Kitamura:1 大石 直也 / Naoya Oishi:2 福山 秀直 / Hidenao Fukuyama:2 高橋 良輔 / Ryosuke Takahashi:1 猪原 匡史 / Masafumi Ihara:3 
  • 1:京都大学大学院医学研究科臨床神経学 / Department of Neurology, Kyoto University Graduate School of Medicine, Japan 2:京都大学大学院医学研究科附属脳機能総合研究センター / Human Brain Research Center, Kyoto University Graduate School of Medicine, Japan 3:国立循環器病研究センター / Department of Stroke and Cerebrovascular Diseases, National Cerebral and Cardiovascular Center, Japan 

Background and Purpose; Rats subjected to bilateral common carotid artery (CCA) occlusion or 2-vessel occlusion (2VO) have been used as animal models of subcortical ischemic vascular dementia (SIVD). However, these models possesses an inherent limitation in that cerebral blood flow (CBF) drops too sharply, and lacks vascular risk factors and causative small vessel changes. We tested the ameroid constrictor device to circumvent such an acute CBF reduction by gradual narrowing of the CCAs of Wistar-Kyoto rats (WKYs) and spontaneous hypertensive rats (SHRs), thus replicating chronic cerebral hypoperfusion more precisely.
Method; Male WKYs and SHRs were each divided into three groups, 2-vessel gradual occlusion (2VGO), where rats were subjected to surgical implantation of ameroid constrictors to the bilateral CCAs, 2VO, and sham control groups. The temporal profiles of CBF, glucose metabolism, spatial working memory and the degrees of histological changes were compared.
Results; The acute CBF reduction and resultant inflammatory responses observed in the 2VO group were eliminated in the 2VGO group by gradual narrowing of the bilateral CCAs; CBF gradually decreased to approximately 70% of baseline level at 3 days post-operation and was still less than 85% at 28 days. Thus, chronic cerebral hypoperfusion was segregated, and induced selective white matter damage with relatively preserved neurovascular coupling and substantially less metabolic and histological derangements in the gray matter including hippocampus. This led to significant spatial working memory impairment of a similar magnitude to the 2VO group at 28 days. SHRs showed more extensive CBF reduction and histological abnormalities in the white matter compared to WKYs.
Conclusions; The 2VGO model, compared with 2VO model, may better mimic cognitive impairment subsequent to selective white matter damage due to chronic cerebral hypoperfusion. SHRs-2VGO model could even more precisely mimic SIVD because of the underlying small vessel pathology.

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