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J Vet Sci. 2007 Dec;8(4):369-376 |
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Canine model of ischemic stroke with permanent middle cerebral artery occlusion: clinical and histopathological findings
Byeong-Teck Kang1,ΆΣ, Jong-Hwan Lee2,ΆΣ, Dong-In Jung1, Chul Park3, Su-Hyun Gu1, Hyo-Won Jeon1, Dong-Pyo Jang5, Chae-Young Lim1, Fu-Shi Quan2, Young-Bo Kim5, Zang-Hee Cho5, Eung-Je Woo4, Hee-Myung Park1,* |
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1Department of Veterinary Internal Medicine, and 2Department of Anatomy, College of Veterinary Medicine, Konkuk University, Seoul 143-701, Korea
3Acupuncture & Meridian Science Research Center and 4College of Electronics and Information, Kyunghee University, Yongin 446-701, Korea
5Neuroscience Research Institute, Gachon University of Medicine and Science, Incheon 405-760, Korea
* parkhee@konkuk.ac.kr |
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The aim of the present study was to assess the clinical
and histopathological findings in a canine model of ischemic
stroke. Cerebral ischemic stroke was induced by middle
cerebral artery occlusion in four healthy beagle dogs
using silicone plugs. They showed neurological signs of
forebrain dysfunction such as reduced responsiveness,
head turning, circling, postural reaction deficits, perceptual
deficits, and hemianopsia. These signs gradually regressed
within 4 weeks without therapy. On magnetic resonance
imaging, T2 hyperintensity and T1 hypointensity
were found in the cerebral cortex and basal ganglia. These
lesions were well-defined and sharply demarcated from
adjacent brain parenchyma with a homogenous appearance.
No abnormalities of the cerebrospinal fluid were
observed. At necropsy, atrophic and necrotic lesions were
observed in the cerebral cortex. The cerebral cortex, basal
ganglia, and thalamus were partially unstained with triphenyl-
tetrazolium chloride. Histopathologically, typical
features of infarction were identified in cortical and thalamic
lesions. This study demonstrates that our canine model
resembles the conditions of real stroke patients.
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