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背景:脑缺血后兴奋性氨基酸过量释放是引起继发性脑损伤的主要原因之一,但是脑缺血后谷氨酸能神经元的形态学变化详尽报道较少。目的:观察脑缺血15min～6h内缺血区,谷氨酸能神经元的变化规律。设计:非随机对照的实验研究。地点和对象:实验地点:河北工程学院。选取雄性健康SD大鼠48只,体质量280～350g。干预:按插线法制备大鼠局灶性脑缺血模型,分为梗死15,30min,1,2,3,6h组,分别进行灌注固定后,取脑组织块进行冰冻冠状切片,每隔15片取两片,分成两套,一套进行ABC免疫组织化学反应,另一套做阴性对照试验。主要观察指标:缺血区和非缺血区免疫组织化学染色结果、阴性对照试验切片结果。结果:缺血15min～1h,缺血中心区即出现阳性细胞,且逐渐增加,胞质染色加深,主要分布于大脑皮质Ⅲ～Ⅴ层,以锥体细胞为主,苍白球内侧部,尾壳核也有少量阳性细胞。缺血2h其数量减少,染色较淡;缺血6h阳性细胞消失。同时观察到阳性细胞由缺血中心区逐渐向半影区(边缘区)扩展。结论:脑缺血早期谷氨酸能神经元大量合成、释放谷氨酸导致神经元损伤,同时为临床治疗脑梗死及早用药提供依据。
BACKGROUND: Excessive release of excitatory amino acids after cerebral ischemia is one of the major causes of secondary brain injury. However, morphological changes of glutamatergic neurons after cerebral ischemia are reported in detail. Objective: To observe the changes of ischemic and glutamatergic neurons within 15min to 6h after cerebral ischemia. Design: Non-randomized controlled experimental study. Location and object: Experiment Location: Hebei Institute of Technology. 48 male healthy SD rats were selected and their body weight was 280 ~ 350g. Intervention: Focal cerebral ischemia model was made according to the patch cord method and divided into 15, 30 min, 1, 2, 3 and 6 h after infarction. After perfusion and fixation, the brain tissue was frozen and coronal sectioned. Take 15 pieces of two, divided into two sets, a set of ABC immunohistochemical reaction, another set of negative control test. MAIN OUTCOME MEASURES: Immunohistochemical staining of ischemic area and non-ischemic area, results of negative control test. Results: In the ischemic 15min ~ 1h, positive cells appeared in the ischemic center area, and gradually increased, the cytoplasm staining deepened, mainly distributed in the cerebral cortex Ⅲ ~ Ⅴ layer, the main pyramidal cells, globus pallidus medial part, the tail shell The nucleus also has a small amount of positive cells. Ischemia 2h its number decreased, staining lighter; Ischemia 6h positive cells disappear. At the same time, it was observed that the positive cells gradually expanded from the ischemic center to the penumbra (marginal zone). Conclusion: In the early stage of cerebral ischemia, glutamate neurons are synthesized in a large amount and glutamate is released to cause neuronal damage. At the same time, it provides a basis for clinical treatment of cerebral infarction and early administration.