Evolution of photochemically induced focal cerebral ischemia in the rat - Magnetic resonance imaging and histology
Evolution of photochemically induced focal cerebral ischemia in the rat - Magnetic resonance imaging and histology
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DOI：
10.1161/01.str.27.11.2110
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发表时间：
1996-11-01
期刊：
影响因子：
8.3
通讯作者：
James, MF
中科院分区：
文献类型：
--
作者：
Lee, VM;Burdett, NG;James, MF
背景与目的磁共振成像（MRI）越来越多地用于研究人类和动物脑缺血的病理生理演变。我们研究了光化学诱导的局灶性脑缺血，这是一种相对无创的脑缺血。并分别用MRI和组织学比较了脑缺血反应在体内和死后的演变。方法对34只成年雄性蒙氏大鼠进行双侧缺血诱导后7个时间点（3.75 ~ 196 h）的T-2、弥散、T-2*加权MR图像、甲酚快紫外（CFV）染色平行切片和胶质原纤维酸蛋白切片。根据CFV组织学，计算病变体积和细胞计数；从弥散加权和t -2加权图像中，确定病变体积。结果放射后3.75小时，MRI和组织学显示病灶清晰，时间演变规律一致；病变表观扩散系数在3.75 h时显著降低，在第2天显著升高，且与病变cfv阳性细胞数下降显著相关。第2天，星形胶质细胞和结缔组织细胞侵入梗死区。在整个时间过程中，体内和死后（收缩校正后）测定的病变体积吻合良好。结论MRI变化定量反映了组织病理学，无创性地揭示了可重复的原发性和继发性损伤特征。这些变化基本上重复了其他动物脑卒中模型和临床报道，强调了MRI和光化学诱导局灶性脑缺血模型在脑卒中研究中的价值。
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 T-2, diffusion, and T-2* 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 T-2-weighted images, 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.