Objective   To observe the pathological characteristics of brain injuries of rats exposed to blast high acceleration in airtight cabin and to study the relevant mechanism.  Methods   Columnar explosive in a metal energy concentration disk under airtight cabin was detonated

imitating armored vehicle mine blast

to establish a model of brain injuries induced by blast high acceleration in airtight cabin. Forty-eight rats were randomly divided into control group

400 mg TNT explosion equivalent group (400 mg group) and 800 mg TNT explosion equivalent group (800 mg group)

16 rats in each group. Eight rats in each injury group were used to record the peak acceleration (PA) and the time of acceleration duration (TD) of the seat and skull as evaluation indexes of the acceleration load on the rats. Six hours after explosion

pathological changes of spinal cord and brain tissues in rats were examined under light microscope or transmission electron microscope (TEM). Meanwhile

the number of intact pyramidal cells per 1 mm linear length of CA1 was determined and neuronal damage to the hippocampal CA1 subfield was semi-quantitatively graded using a 0-3 rating system according to the method of Kato et al. The spatial learning and memory of another 8 rats were assessed with Morris water maze (MWM) after explosion.  Results   The PA and TD of seat were （5 745±1 036）g and （6.87±0.58）ms

（701±309） g and （1.00±0.14）ms of skull respectively in 400 mg group

（13 109±1167）g and（11.08±1.43）ms

（3 383±935）g  and （1.32±0.18）ms of skull respectively in 800 mg group (P0.01）. No visible change was observed in brain of injury groups

but acute neuronal damage to cerebral cortex

hippocampus and spinal cord was observed under microscope. Damage to capillary and axon was observed in 800 mg group under TEM. The damage score was the highest in 800 mg group and the lowest in control group. The neuronal density of hippocampal CA1 subfield was the lowest in 800 mg group and the highest in control group (P0.01). During the first 4 d after explosion

the escape latency was significantly longer in 800 mg group than in control group (P0.05). The learning and memory curve was shifted right in 800 mg group and became stable after 1 d. The frequency of crossing the target platform was lower and the time spent in crossing the target quadrant was longer in 800 mg group than in control group (P0.05). The value of these 2 parameters was a median in 400 mg group.  Conclusion   Rats exposed to blast high acceleration in airtight cabin may suffer from mild diffused brain injury which may induce early clinical symptoms or late sequel. Occupants may suffer from brain injuries while armored vehicles can be attacked by landmines in the absence of a bottom penetration and large displacement

which should attract more attention of armored vehicle designers and clinicians.