Su-Hyun Gu

Canine model of ischemic stroke with permanent middle cerebral artery occlusion: clinical and histopathological findings

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.

Detection of cerebral metabolites in a canine model of ischemic stroke using 1H magnetic resonance spectroscopy.

Proton magnetic resonance spectroscopy ((1)H MRS) provides in vivo biochemical information on tissue metabolites. The purpose of this study was to investigate the serial metabolic changes of (1)H MRS in the cerebrum of ischemic dogs. An ischemic stroke was induced in five health laboratory beagle dogs by permanent middle cerebral artery occlusion using a silicone plug. (1)H MRS was serially performed three times with a 1.5-T MR system: before, three days after and 10days after the stroke. Immunohistochemical staining was performed to determine the expression of neuronal nuclei (NeuN) and glial fibrillary acidic protein (GFAP) at both the ipsilateral and contralateral cerebral cortex. Reduced levels of N-acetyl-asparate (p<0.05), choline (Cho), creatine (Cr) and myo-inositol (mI), and a marked increase in the lactate (Lac) level (p<0.01) were found at three days after the stroke. At 10days after the stroke, the levels of Lac significantly increased (p<0.01); however, the other metabolites were partially elevated. The changes of Cr, Cho and mI were not statistically significant (p>0.05) when the before and after stroke values were compared. There was a significant loss of NeuN and GFAP immunoreactivity at the ischemic core. (1)H MRS may be to a useful diagnostic tool for the evaluation of ischemic stroke in dogs.