BACKGROUND AND PURPOSE: Magnetic resonance imaging (MRI) is increasingly used to study the pathophysiological evolution of cerebral ischemia in humans and animals. We have investigated photochemically induced (rose bengal) focal cerebral ischemia, a relatively noninvasive, reproducible model for stroke, and compared the evolution of the ischemic response in vivo and postmortem with MRI and histology, respectively. METHODS: MR images weighted for T2, diffusion, and T2* and parallel histological sections stained with cresyl fast violet (CFV) and for glial fibrillary acid protein were obtained from 34 adult male Hooded Lister rats at seven time points (3.75 to 196 hours) after bilateral ischemia induction. From CFV histology, lesion volumes and cell counts were calculated; from diffusion-weighted and T2-weighted images, apparent diffusion coefficients and lesion volumes were determined. RESULTS: Both MRI and histology revealed a well-defined lesion at 3.75 hours after irradiation and a consistent pattern of temporal evolution; lesion apparent diffusion coefficients decreased significantly by 3.75 hours, increased significantly by day 2, and correlated strikingly with the decline in lesion CFV-positive cell numbers. After day 2, astrocytes and connective tissue cells invaded the infarct. Throughout the time course, lesion volumes determined in vivo and postmortem (after shrinkage correction) agreed well. CONCLUSIONS: MRI changes quantitatively reflect histopathology, revealing reproducible primary and secondary damage characteristics noninvasively. These changes essentially replicate those reported for other animal stroke models and clinically, emphasizing the value both of MRI and the photochemically induced focal cerebral ischemia model in stroke research.
BACKGROUND AND PURPOSE: Magnetic resonance imaging (MRI) is increasingly used to study the pathophysiological evolution of cerebral ischemia in humans and animals. We have investigated photochemically induced (rose bengal) focal cerebral ischemia, a relatively noninvasive, reproducible model for stroke, and compared the evolution of the ischemic response in vivo and postmortem with MRI and histology, respectively. METHODS: MR images weighted for T2, diffusion, and T2* and parallel histological sections stained with cresyl fast violet (CFV) and for glial fibrillary acid protein were obtained from 34 adult male Hooded Lister rats at seven time points (3.75 to 196 hours) after bilateral ischemia induction. From CFV histology, lesion volumes and cell counts were calculated; from diffusion-weighted and T2-weighted images, apparent diffusion coefficients and lesion volumes were determined. RESULTS: Both MRI and histology revealed a well-defined lesion at 3.75 hours after irradiation and a consistent pattern of temporal evolution; lesion apparent diffusion coefficients decreased significantly by 3.75 hours, increased significantly by day 2, and correlated strikingly with the decline in lesion CFV-positive cell numbers. After day 2, astrocytes and connective tissue cells invaded the infarct. Throughout the time course, lesion volumes determined in vivo and postmortem (after shrinkage correction) agreed well. CONCLUSIONS: MRI changes quantitatively reflect histopathology, revealing reproducible primary and secondary damage characteristics noninvasively. These changes essentially replicate those reported for other animal stroke models and clinically, emphasizing the value both of MRI and the photochemically induced focal cerebral ischemia model in stroke research.
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