Stroke location and brain function in an embolic rabbit stroke model.
Stroke location and brain function in an embolic rabbit stroke model.
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DOI：
10.1016/j.jvir.2010.02.023
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发表时间：
2010-06
影响因子：
2.9
通讯作者：
Culp, William C.
中科院分区：
文献类型：
--
作者：
Brown, Aliza T.;Skinner, Robert D.;Flores, Rene;Hennings, Leah;Borrelli, Michael J.;Lowery, John;Culp, William C.
目前的兔中风模型通常依赖于症状作为栓塞的终点，并且在中风的位置、大小和严重程度上产生广泛的变化。为了进一步完善我们的血管造影栓塞性卒中模型，我们将局部梗死与神经功能缺损相关联。我们的目标是建立一个用于中风后长期治疗研究的兔模型。新西兰白色兔（4-5 kg）（n=71）进行选择性颈内动脉（伊卡）血管造影，并注射单个凝块。在24小时时，在0=正常至10=死亡量表上测量神经系统评估评分（NAS）。取出大脑并染色以识别中风区域。所有单次中风的动物，N=31，通过特定的脑结构参与和NAS值进行相关分析。卒中发生率因部位而异，皮质、皮质下和基底节区最高。大脑中动脉（MCA）和大脑前动脉（ACA）分布最常见，分别为52%和29%，ACA分布中每搏输出量最大。脑干和小脑卒中具有不成比例的严重神经功能缺损，NAS评分为2.25±1.0，而皮质（0.5±0.2）、皮质下（1.3±0.4）和基底节（0.5±0.3）均位于额叶或顶叶区域（P≤0.02）。MCA和ACA分布包括81%的卒中。这些部位相对沉默（可能允许长期生存研究），而后循环中的其他部位则产生不成比例的严重症状。症状不是卒中发生的可靠指标，可能需要其他终点，如成像。这些都是改善兔中风模型的重要步骤。
Current rabbit stroke models often depend on symptoms as endpoints for embolization and produce wide variation in location, size, and severity of strokes. To further refine our angiographic embolic stroke model we correlated localized infarctions to neurological deficits. Our goal is a rabbit model for long term studies of therapies after stroke. New Zealand White rabbits (4–5 kg) (n=71) had selective internal carotid artery (ICA) angiography and a single clot was injected. At 24 hours neurological assessment scores (NAS) were measured on a 0=normal to 10=dead scale. Brains were removed and stained to identify stroke areas. All animals with single strokes, N=31, were analyzed by specific brain structure involvement and NAS values were correlated. Stroke incidence differed by location with cortex, subcortical, and basal ganglia regions highest. Distributions of middle cerebral artery (MCA) at 52% and anterior cerebral artery (ACA) at 29% were most commonly involved with largest stroke volumes in the ACA distribution. Brain stem and cerebellum strokes had disproportionately severe neurological deficits, scoring 2.25±1.0 vs. cortex (0.5±0.2), subcortical (1.3±0.4) and basal ganglia (0.5±0.3) all in the frontal or parietal regions on NAS (P≤0.02). MCA and ACA distributions included 81% of strokes. These sites were relatively silent (potentially allowing longer term survival studies) while others in the posterior circulation produced disproportionately severe symptoms. Symptoms were not reliable indicators of stroke occurrence and other endpoints such as imaging may be required. These are important steps towards refinement of the rabbit stroke model.
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