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背景:应用大鼠脑缺氧耐受实验可以认识内源性神经保护机制。目的:观察脑缺氧预处理大鼠模型的脑缺氧耐受特点。设计:随机对照动物实验。单位:吉林大学中日联谊医院神经内科。材料:实验于2003-04/2004-04在吉林大学中日联谊医院基础动物实验中心完成。纯系健康Wistar大鼠,随机分为正常对照组、假手术组,6只/组;缺血对照组,20只,预缺氧(3h,8%O2和92%N2)+缺血组:60只,根据缺氧时间不同分为5个时相点,即30min,1,3,5,6h点,每个时相点12只大鼠。预缺氧组:18只,根据缺氧时间不同分为3个时相点,即1,3,5h点,每个时相点6只大鼠(3只用于TTC染色,3只用于苏木精-伊红)。方法:①缺氧预处理:在固定体积的密闭玻璃容器中,首先放入钠石灰吸收二氧化碳和氧气,然后输入8%O2和92%N2的混和气体,放入动物,3只/次。并尽量保持温度、湿度恒定。②建立大鼠大脑中动脉永久性缺血模型。③通过神经病学评分、梗死体积判定、病理标本制作、免疫组织化学染色、图像分析等一系列步骤对该模型进行评价。④组间比较采用方差分析。主要观察指标:实验组和对照组大鼠脑梗死体积、神经病学评分及病理形态学改变。结果:预缺氧(8%O2,1,3,5h)+缺血组神经功能评分,低于缺血对照组(P<0.01)。缺氧8%O2,30min及6h)组神经功能评分,与缺血对照组相比差异无显著性(P>0.05)。预缺氧(8%O2,1,3,5h)+缺血组脑梗死平均体积比,低于缺血对照组,(P<0.01)。缺氧(8%O2,30min及6h)组平均梗死体积比为与缺血对照组相比差异无显著性(P>0.05)。结论:大鼠缺氧预处理,能有效减轻局灶性脑缺血所致的神经损伤,具有脑保护作用。用缺氧预处理建立的脑缺血耐受模型操作简便,稳定性好,对实验动物损伤小,是一种研究脑缺血耐受的有用工具。
BACKGROUND: The application of rat cerebral hypoxia tolerance test can recognize the mechanism of endogenous neuroprotection. Objective: To observe the characteristics of hypoxic tolerance of cerebral hypoxic preconditioning rat model. Design: Randomized controlled animal experiments. Unit: Sino-Japanese Friendship Hospital, Jilin University, Department of Neurology. MATERIALS: Experiments were performed at Basic Animal Experiment Center of China-Japan Friendship Hospital, Jilin University from April 2003 to April 2004. Pure healthy Wistar rats were randomly divided into normal control group, sham operation group, 6 rats / group, ischemic control group, 20 rats, hypoxic (3h, 8% O2 and 92% N2) 60, according to different hypoxia time is divided into five time points, namely 30min, 1,3,5,6 h, each time point 12 rats. Hypoxia group: 18 rats were divided into 3 time points according to different hypoxia time, namely 1,3,5h point, 6 rats at each time point (3 for TTC staining and 3 for Hematoxylin - Eosin). Methods: ① Anoxia preconditioning: In a fixed volume of airtight glass containers, sodium lime was first taken in to absorb carbon dioxide and oxygen, and then mixed gas of 8% O2 and 92% N2 was put into the animal and 3 / times. And try to keep the temperature and humidity constant. ② Establish a model of permanent middle cerebral artery occlusion in rats. ③ The neurological score, infarction volume determination, pathological specimens, immunohistochemical staining, image analysis and a series of steps to evaluate the model. ④ comparison between groups using analysis of variance. MAIN OUTCOME MEASURES: Changes of cerebral infarction volume, neurological score and pathomorphology in experimental group and control group. Results: The neurological deficit scores of ischemic preconditioning (8% O2, 1, 3, 5h) + ischemia group were lower than those of ischemic control group (P <0.01). Compared with the ischemic control group, there was no significant difference (P> 0.05) in neurological deficit scores of 8% O2, 30min and 6h hypoxia groups. Compared with ischemic control group, the mean volume fraction of ischemic cerebral infarction in preoxygenation (8% O2, 1, 3, 5h) + ischemic group was significantly lower than that in ischemic control group (P <0.01). The mean infarct volume ratio in hypoxia group (8% O2, 30min and 6h) was not significantly different from that in ischemic control group (P> 0.05). Conclusion: The hypoxia preconditioning in rats can effectively reduce the nerve damage induced by focal cerebral ischemia and has the protective effect on the brain. The ischemic tolerance model established by hypoxia preconditioning is simple, stable and has less damage to experimental animals. It is a useful tool to study cerebral ischemic tolerance.