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目的 :探讨急性应激时NO等自由基对脑损害作用及超微结构的影响。方法 :建立急性应激大鼠模型 ,分别取边缘系统额叶、海马、下丘脑组织 ,电镜观察神经细胞超微结构变化、测定组织匀浆NO含量和SOD活力。结果 :急性应激组大鼠额叶、海马及下丘脑SOD活力均高于对照组 (P <0 0 5 ) ,NO含量在海马、下丘脑升高明显 (P <0 0 5 ) ,光镜和电镜下的海马、下丘脑神经细元减少 ,核仁碎裂、胞质内细胞器减少。结论 :急性应激脑组织NO含量和SOD活力增高 ,可对边缘系统下丘脑、海马造成损害。这可能是应激反应过度的病理生理学基础
Objective: To investigate the effects of NO and other free radicals on brain damage and ultrastructure in acute stress. Methods: The rat model of acute stress was established. The ultrastructure of neurons in the frontal lobe, hippocampus and hypothalamus of the limbic system were observed under electron microscope. The content of NO and the activity of SOD in the tissue homogenate were determined. Results: The SOD activity in the frontal lobe, hippocampus and hypothalamus of rats in acute stress group were significantly higher than those in control group (P <0.05). The contents of NO in hippocampus and hypothalamus were significantly increased (P <0.05) And electron microscopy of the hippocampus, hypothalamic neuronal cells reduced, nucleolus fragmentation, decreased cytoplasmic organelles. CONCLUSION: NO content and SOD activity in acute stress brain tissue are increased, which may cause damage to hypothalamus and hippocampus in limbic system. This may be the basis of the pathophysiology of stress reactivity