Neuroelectrophysiological mechanism of disabling brain injury resulting from exposure of rat to blast in a tightly closed compartment

Objective　To explore the dynamic changes in disabling brain injury in a closed compartment, and its underlying neuroelectrophysiological mechanism after exposure of rats to blast. Methods　Sixty-eight SD rats were randomly divided into control group, OTB group ( blast in an open space), and ECB group (blast in a tightly closed compartment). ECB and OTB groups were exposed to blast in a closed chamber simulating the cabin of an armored vehicle and OT (outside of the cabin) with 600-mg detonator electric blasting and 21.5-cm away from the detonating point. The changes of disabled ischemic area of the brain and evoked potential before and 1, 3, 5, 8, 12, 24h and 72h after the blast injury were observed. Results　The incapability score of ECB and OTB rats reached the same level (25%). With 3, 5-triphenyltetrazolium chloride staining, it was found that the infarct area in OTB group appeared 5h after explosion, reaching the climax at 12h, and disappearing at 72h. In the ECB group, the area of infarct appeared 3h after injury, and still existed till 72h after injury. In ECB group, the N1 latency of sensory evoked potential (SEP) and motor evoked potential (MEP) was longer than that of control group 5 and 8 hours after explosion respectively, and the changes in sensation appeared earlier than those of motor function. Conclusions　The blast wave in EC shows a characteristic of a complex blast wave, and its damage to the brain can be more severe, which is caused more by ECB than by OTB. The size of infarct area and latency of evoked potential might contribute to the brain incapability. DOI: 10.11855/j.issn.0577-7402.2015.08.13