Petito C K
Stroke. 1979 Mar-Apr;10(2):192-6. doi: 10.1161/01.str.10.2.192.
Cerebral infarction was produced in paralyzed, ventilated rats by a 30 min period of right common carotid artery occlusion combined with systemic hypoxia (Pao2 21-25 mm Hg). After 30 min the arterial clamp was removed and the animals were reoxygenated and allowed to survive for 1 min (6 animals), 30 min (12 animals), or 1 1/2 to 2 h (6 animals). The animals were reanesthetized and sacrificed by perfusion-fixation with paraformaldehyde-glutaraldehyde. Light and electron microscopy revealed ischemic cell change in neurons in the ipsilateral cerebral cortex, striatum and hippocampus. These changes were mild to moderate in the early post-ischemic period and severe in the post-ischemic period. Cerebral infarction was present in one of the 30 min survivors and in all of the 1 1/2 to 2 h survivors. Electron microscopy showed platelet thrombi in the infarcted brain in 3 of the 7 animals with infarcts, and in an area of very severe ischemic cell change in a fourth animal. They were not present in areas of brain showing only mild to moderate ischemic cell change. These findings showed that platelet thrombi form in association with cerebral infarcts and suggested that they are induced by tissue necrosis rather than by neuronal ischemic cell change alone.
通过夹闭右侧颈总动脉30分钟并结合全身缺氧(动脉血氧分压21 - 25 mmHg),在瘫痪且使用呼吸机的大鼠中制造脑梗死。30分钟后移除动脉夹,使动物再给氧,并存活1分钟(6只动物)、30分钟(12只动物)或1.5至2小时(6只动物)。再次对动物进行麻醉,并用多聚甲醛 - 戊二醛灌注固定处死。光镜和电镜检查显示,同侧大脑皮质、纹状体和海马体中的神经元出现缺血性细胞改变。这些改变在缺血后早期为轻度至中度,在缺血后期则较为严重。在存活30分钟的动物中有1只出现脑梗死,在存活1.5至2小时的动物中全部出现脑梗死。电镜检查显示,在7只发生梗死的动物中有3只在梗死脑区出现血小板血栓,在第4只动物的非常严重的缺血性细胞改变区域也出现血小板血栓。在仅表现为轻度至中度缺血性细胞改变的脑区未发现血小板血栓。这些发现表明,血小板血栓与脑梗死相关形成,提示它们是由组织坏死而非仅由神经元缺血性细胞改变诱导产生。