Ultrastructural and functional characteristics of blast injury-induced neurotrauma

Objective: The present study investigates whether whole-body or local (ches t) 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 d ays. 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 f ocused on the right middle thoracic region and generated by small-scale sho ck tube (n = 40) while the heads of animals were protected, At the completi on of cognitive testing, rats were killed at 3 hours, 24 hours, and 5 days after injury. Ultrastructural changes in the hippocampus were analyzed elec tron microscopically. Parameters of oxidative stress (malondialdehyde and s uperoxide anion generation) and antioxidant enzyme defense (superoxide dism utase 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 demon strated swellings of neurons, glial reaction, and myelin debris in the hipp ocampus. AII rats revealed significant deficits in performance of the activ e avoidance task 3 hours after injury, but deficits persisted up to day 5 a fter injury only in rats subjected to WBBI, Oxidative stress development an d altered antioxidant enzyme defense was observed in animals in both groups . Cognitive impairment and biochemical changes in the hippocampus were sign ificantly correlated with blast injury severity in both WBBI and LBI groups . Conclusion: These results confirm that exposure to blast overpressure induc es ultrastructural and biochemical impairments in the brain hippocampus, wi th associated development of cognitive deficits.