These results confirm that exposure to blast overpressure induces ultrastructural and biochemical impairments in the brain hippocampus, with associated development of cognitive deficits.

Blast injuries, that is injuries caused by the complex pressure wave generated by some explosions, show increasing frequency throughout the world. However, whether blast injury is capable of inducing memory dysfunction has not been previously investigated. The present study examines the effects of blast injury-induced neurotrauma on memory deficit in rats. Furthermore, it is hypothesized that blast injury, stimulating nitric oxide production in the medial mesodiencephalic reticular formation and the dorsal hippocampus, both structures being involved in memory processing, may induce memory deficits. Prior to blast injury, 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, using a BT-I shock tube. Neurotrauma was confirmed by electron microscopical examination. At the completion of cognitive testing, rats were sacrificed at 3, 24 hours and 5 days after injury. The nitric oxide production in the brain structures was determined by the total nitrite/nitrate concentration, and by the expression of inducible nitric oxide synthase mRNA. The rats with blast injury revealed significant deficits in performance of the active avoidance task that persisted up to 5 days post-injury. Electron microscopical findings in both brain structures showed swellings of neurons, glial reaction, myelin debris, and increased pinocytotic activity on the fifth day following trauma. In blast injured rats, there was a significant elevation in total nitrite/nitrate levels 3 and 24 hours following injury which was comparable with the changes in the expression of inducible nitric oxide synthase mRNA. The results indicate that blast injury-induced neurotrauma is able to cause cognitive deficits.

The local, general, and cerebral responses of rabbits exposed to pulmonary blasts were examined to define the role of vagal afferentation in cardiorespiratory as well as metabolic control after a blast injury. Two series of experiments were conducted on rabbits to analyze the general, local, and cerebral responses to pulmonary injury caused by blast overpressure, and to evaluate the effects of bilateral vagotomy on the general, local, and cerebral responses to local (pulmonary) blast injury. The blast wave was generated in laboratory conditions using an air-driven shock tube that was able to cause moderate pulmonary blast injury, i.e., four pulmonary contusions characterized as confluent ecchymoses involving 30 to 60% of the lungs. One group of animals was subjected to pulmonary deafferentation, performed by bilateral transections of the vagus, glossopharyngeal, and hypoglossal nerves. Numerous hemodynamic as well as biochemical parameters were observed in systemic circulation and in lung and brain (medulla oblongata) tissues. After observation during the early posttraumatic period, rabbits were sacrificed by decapitation 30 minutes after the blast injury. On the basis of obtained results, it was concluded that vagal afferents have an important role in the modification of general and local responses to a pulmonary blast injury. Furthermore, it was suggested that functional changes in medulla oblongata may be the consequences of afferent neural impulses from the injured region (lungs) rather than consequences of ischemia, energy transfer to the brain, or both.

In relation to the immediate management of patients injured by explosive weapons, it follows that particular attention should be paid to the presence and/or development of blast injury. Our findings indicate that blast is more common in war injuries than previously thought. Eicosanoid changes after blast injury suggest that blast injury causes a major physiologic stress. A variety of effects on the central nervous system suggest that blast injury could be responsible for some aspects of what is now considered to be the posttraumatic stress disorder.