RESUMO
Objective To observe the characteristics of rat brain injury induced by shock wave propagation in solids resulting from underwater explosion and explore the related mechanism. Methods Explosion source outside the simulated ship cabin underwater was detonated for establishing a model of brain injury in rats by shock wave propagation in solid; 72 male SD rats were randomly divided into normal control group (n=8), injury group 1 (600mg RDX paper particle explosion source, n=32), injury group 2 (800mg RDX paper particle explosion source, n=32). The each injury group was randomly divided into 4 subgroups (n=8), 3, 6, 24 and 72h groups. The division plate as a whole and the head of 8 rats in each injury group were measured for the peak value of the solid shock wave, its rising time and the duration time of shock wave propagation in solid. To observe the physiological changes of animals after injury, plasma samples were collected for determination of brain damage markers, NSE and S-100 β. All the animals were sacrificed, the right hemisphere of the brain was taken in each group of animals, weighting after baking, and the brain water content was calculated. Pathological examination was performed for left cerebral hemisphere in 24-h group. The normal pyramidal cells in the hippocampal CA1 region were counted. Results The peak value, rising time and duration time of shock wave propagation on the division plate and head were 1369.74± 91.70g, 0.317± 0.037ms and 24.85± 2.53ms, 26.83± 3.09g, 0.901± 0.077ms and 104.21± 6.26ms respectively in injury group 1, 1850.11± 83.86g, 0.184± 0.031ms and 35.61± 2.66ms, 39.75± 3.14g, 0.607± 0.069ms and 132.44± 7.17ms in injury group 2 (P<0.01). After the injury, there was no abnormality in the anatomy, and brain damage markers NSE, S-100 β increased, reached the peak at 24 h, and they were highest in injury group 2 and lowest in control group with a statistically significant difference (P<0.05). The brain water content increased, reached the peak at 24h, and was the highest in injury group 2 and the lowest in control group with a statistically significant difference (P<0.05). No visible change was observed in the brain of injury groups, but acute neuronal damages to the cerebral cortex and hippocampus were observed under microscope. The neuronal density of hippocampal CA1 subfield was the lowest in injury group 2 and the highest in control group (P<0.05). Conclusions Shock wave propagation in solids from underwater explosion may lead to pathological changes such as brain edema and neuronal degeneration in rats, and cause mild traumatic brain injury in rats, thus, it is essential to strengthen prevention and care.