密闭舱室内爆炸致大鼠失能性脑损伤的神经电生理机制研究

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

目的探讨密闭舱室内爆炸致大鼠失能性脑损伤的动态变化规律及神经电生理机制。方法 68只SD大鼠随机分为正常对照组(n=4)、开阔地爆炸组(OTB组,n=32)和舱室爆炸组(ECB组,n=32)。舱室爆炸组和开阔地爆炸组分别在模拟装甲舱室内和舱外以600mg雷管电起爆,动物距爆点21.5cm。观察大鼠伤前及伤后1、3、5、8、12、24、72h(每个时间点4只大鼠)失能性脑缺血面积和诱发电位的改变。结果舱室内、外爆炸后30min大鼠失能程度均为25%。TTC染色显示开OTB组伤后5h出现肉眼可见脑缺血区域,12h缺血区面积最大,至72h基本恢复正常;ECB组伤后3h即可见缺血区,至72h缺血区仍存在。诱发电位检测显示,ECB组伤后5h体感诱发电位N1波潜伏期延长,伤后8h运动诱发电位N1波潜伏期延长,且感觉变化先于运动变化。结论舱室爆炸致脑失能较开阔地爆炸更早且伤情更重,缺血区域和诱发电位的潜伏期可能与失能性脑损伤相关。

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.