Ultrastructural and functional characteristics of blast injury-induced neurotrauma
Ultrastructural and functional characteristics of blast injury-induced neurotrauma
复制标题
爆炸损伤引起的神经损伤的超微结构和功能特征
DOI：
10.1097/00005373-200104000-00017
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发表时间：
2001-04-01
影响因子：
--
通讯作者：
Savic, J
中科院分区：
文献类型：
--
作者：
Cernak, I;Wang, ZG;Savic, J
目的：本研究调查是否全身或局部（胸部）暴露于爆炸超压可以诱导超微结构，生化和认知障碍在brain.Methods：雄性Wistar大鼠进行了训练的主动回避任务6天。在第6天，获得回避反应的大鼠（n = 40）经受由大型激波管产生的全身冲击伤（WBBI）;或局部（胸部）冲击伤（LBI），由集中在右胸中部的冲击波超压引起，并由小型冲击管产生（n = 40），同时保护动物的头部。在认知测试完成时，在损伤后3小时、24小时和5天处死大鼠。电镜下观察海马超微结构变化。氧化应激（丙二醛和超氧阴离子生成）和抗氧化酶防御（超氧化物歧化酶和谷胱甘肽过氧化物酶活性）的参数进行了测量，以评估在脑生化变化后blast.Results：在动物进行WBBI或LBI的超微结构研究结果表明，神经元，神经胶质反应，和髓鞘碎片在海马的selling。损伤后3小时，所有大鼠均表现出明显的主动回避功能缺陷，但只有WBBI组大鼠的主动回避功能缺陷持续至损伤后第5天。在两组动物中均观察到氧化应激发展和抗氧化酶防御的改变。认知功能障碍和生化变化在海马显着相关的冲击伤严重程度WBBI和LBI groups.Conclusion：这些结果证实，暴露于爆炸超压诱导脑海马超微结构和生化损伤，与相关的发展认知功能障碍。
Objective: The present study investigates whether whole-body or local (chest) exposure to blast overpressure can induce ultrastructural, biochemical, and cognitive impairments in the brain.Methods: Male Wistar rats were trained for an active avoidance task for 6 days. On day 6, rats that had acquired the avoidance response were subjected to whole-body blast injury (WBBI), generated by large-scale shock tube (n = 40); or local (chest) blast injury (LBI), induced by blast overpressure focused on the right middle thoracic region and generated by small-scale shock tube (n = 40) while the heads of animals were protected, At the completion of cognitive testing, rats were killed at 3 hours, 24 hours, and 5 days after injury. Ultrastructural changes in the hippocampus were analyzed electron microscopically. Parameters of oxidative stress (malondialdehyde and superoxide anion generation) and antioxidant enzyme defense (superoxide dismutase and glutathione peroxidase activity) were measured in the hippocampus to assess biochemical changes in the brain after blast.Results: Ultrastructural findings in animals subjected to WBBI or LBI demonstrated swellings of neurons, glial reaction, and myelin debris in the hippocampus. AII rats revealed significant deficits in performance of the active avoidance task 3 hours after injury, but deficits persisted up to day 5 after injury only in rats subjected to WBBI, Oxidative stress development and altered antioxidant enzyme defense was observed in animals in both groups. Cognitive impairment and biochemical changes in the hippocampus were significantly correlated with blast injury severity in both WBBI and LBI groups.Conclusion: These results confirm that exposure to blast overpressure induces ultrastructural and biochemical impairments in the brain hippocampus, with associated development of cognitive deficits.