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目的:选用脂质过氧化抑制剂(U74389F)作为脑保护剂,观察其对大鼠全脑缺血后的海马CA1区诱发电位的影响。方法:雄性SD大鼠20只,随机分三组:对照组(6只),缺血组(7只)与治疗组(7只)均脑缺血10分钟,再灌注7小时,治疗组缺血前1小时腹腔注射U74289F 10mg/kg。结果:大鼠全脑缺血再灌注6小时后,海马诱发电位中兴奋性突触后电位(EPSP)的斜率与缺血前相比显著增加(P<0.05)。治疗组缺血再灌注6小时后EPSP的斜率与缺血组同期相比显著减小(P<0.05)。结论:缺血再灌注6小时后海马CA1区的神经元突触功能毒性增强,而U74389F能有效降低此毒性增强作用,从电生理学角度说明了脑保护作用。
AIM: To investigate the effects of lipid peroxidation inhibitor (U74389F) on the evoked potentials of hippocampal CA1 region after global cerebral ischemia in rats. Methods: Twenty male Sprague-Dawley rats were randomly divided into three groups: control group (6), ischemia group (7) and treatment group (7) for 10 minutes after cerebral ischemia, reperfusion for 7 hours, One hour before blood injection, U74289F 10 mg / kg was injected intraperitoneally. Results: After six hours of global cerebral ischemia-reperfusion, the slope of excitatory postsynaptic potential (EPSP) in hippocampal evoked potential increased significantly compared with that before ischemia (P <0.05). The slope of EPSP in the treatment group 6 hours after ischemia-reperfusion was significantly decreased compared with the same period of ischemia group (P <0.05). CONCLUSION: Neuronal synaptic functional toxicity of hippocampal CA1 region is enhanced 6 h after ischemia-reperfusion, while U74389F can effectively reduce this toxicity enhancement effect. The neuroprotective effect is elucidated electrophysiologically.