Rice J E, Vannucci R C, Brierley J B
Ann Neurol. 1981 Feb;9(2):131-41. doi: 10.1002/ana.410090206.
Brain damage in the Levine preparation (unilateral common carotid artery ligation with hypoxia) consists of ischemic neuronal alterations in the ipsilateral forebrain. As the model has been restricted to adult animals, unilateral common carotid artery ligation was carried out in 7-day-postnatal rats. Four to 8 hours later the 25 pups were exposed to 8% oxygen at 37 degrees C for 3.5 hours. Controls consisted of littermates subjected to carotid ligation without subsequent hypoxia, hypoxia without prior ligation, and neither ligation nor hypoxia. After hypoxia the animals were returned to their dams and appeared normal for up to 50 hours. All pups were then killed by perfusion-fixation. Moderate to severe ischemic neuronal changes were seen in the ipsilateral cerebral cortex, striatum, and hippocampus in at least 90% of the animals and included infarction in 56% of the brains. Cortical damage was occasionally laminar but more often occurred in columns at right angles to the pial surface. Unlike adult animals, there was necrosis of white matter, greater ipsilaterally, originating in and spreading from myelinogenic foci. The evolution of ischemic cell change and the associated gliomesodermal reaction was more rapid than in the adult. In 22 additional pups subjected to carotid artery ligation and hypoxia, brains were analyzed for water content. Significant increases (0.6 to 3.3%) in water content of the ipsilateral hemispheres occurred in 11 of 22 brains (50%). Unilateral ischemia combined with hypoxia in developing rats therefore results in neuronal destruction in the same brain regions as in adult animals, but also causes necrosis of white matter. The incidence of increased water content was similar to that of overt infarction. Thus, as previously shown in the adult, brain edema is a consequence rather than a cause of major ischemic damage in the immature animal.
莱文模型（单侧颈总动脉结扎合并缺氧）导致的脑损伤表现为同侧前脑的缺血性神经元改变。由于该模型仅限于成年动物，因此在出生后7天的大鼠中进行单侧颈总动脉结扎。4至8小时后，将25只幼崽在37摄氏度下暴露于8%的氧气中3.5小时。对照组包括未经历后续缺氧的颈动脉结扎同窝幼崽、未预先结扎仅经历缺氧的同窝幼崽以及既未结扎也未经历缺氧的同窝幼崽。缺氧后，将动物放回母鼠身边，在长达50小时内看起来正常。然后所有幼崽通过灌注固定处死。至少90%的动物在同侧大脑皮层、纹状体和海马体中出现中度至重度缺血性神经元变化，其中56%的大脑出现梗死。皮质损伤偶尔呈层状，但更常见于与软脑膜表面成直角的柱状区域。与成年动物不同，白质出现坏死，同侧更严重，起源于髓鞘形成灶并从该处扩散。缺血性细胞变化及相关的神经胶质中胚层反应的进展比成年动物更快。在另外22只接受颈动脉结扎和缺氧处理的幼崽中，对大脑进行了含水量分析。22只大脑中有11只（50%）同侧半球含水量显著增加（0.6%至3.3%）。因此，发育中的大鼠单侧缺血合并缺氧会导致与成年动物相同脑区的神经元破坏，但也会导致白质坏死。含水量增加的发生率与明显梗死的发生率相似。因此，如先前在成年动物中所显示的，脑水肿是未成熟动物严重缺血性损伤的结果而非原因。
