目的观察爆炸致舱内大鼠高加速度负载时脑损伤的病理特点,探讨其相关机制。方法引爆密闭舱室下方聚能盘内点爆源,模拟装甲车触雷爆炸,制作爆炸致舱内大鼠(坐姿)高加速度负载时脑损伤模型;48只SD雄性大鼠随机分为对照组、400mgTNT爆炸当量致伤组(400mg组)及800mgTNT爆炸当量致伤组(800mg组),每组16只,其中8只用于测量舱室内座位与大鼠头颅的加速度峰值(PA)及持续作用时间(TD),于伤后6h处死,取脑、脊髓组织行病理检查,对海马CA1区正常锥体细胞记数及组织损伤分级,另8只行Morris水迷宫实验检测大鼠空间学习记忆功能。结果 400mg组PA座位为(5745±1036)g,TD座位为(6.87±0.58)ms,PA头颅为(701±309)g,TD头颅为(1.00±0.14)ms;800mg组PA座位为(13109±1167)g,TD座位为(11.08±1.43)ms,PA头颅为(3383±935)g,TD头颅为(1.32±0.18)ms,两组数据对应参数之间差异显著(P<0.01)。伤后6h大鼠大体解剖无明显异常,但光镜下大脑、脊髓存在神经元急性损伤改变,800mg组电镜下还见大脑毛细血管、轴索损伤。海马CA1组织学损伤分级:800mg组>400mg组>对照组;神经元密度:800mg组<400mg组<对照组(P<0.01)。与对照组比较,第1～4天800mg组逃避潜伏期延长(P<0.05),学习记忆曲线右移,延后1d趋于稳定,经过平台次数及跨越目标象限时间减少(P<0.05);400mg组介于两者之间。结论爆炸致舱内大鼠高加速度负载时大鼠可出现轻度弥漫性脑损伤,可能产生相应的早期症状或晚期后遗症,可推得装甲车辆触雷爆炸底板未击穿、变形小时乘员存在脑损伤可能。 Objective To observe the pathological features of brain injury induced by high explosive load in rats and explore the related mechanism. Methods The detonation source in the converging plate below the airtight chamber was detonated to simulate the explosion of the armored vehicle and the model of brain injury caused by high explosive loading in the rats was established. 48 male Sprague-Dawley rats were randomly divided into control group, 400mgTNT (400mg group) and 800mgTNT explosive equivalent wounding group (800mg group), 16 in each group, of which 8 were used to measure the peak acceleration (PA) and duration of action TD) were sacrificed at 6h after injury. Pathological examination of the brain and spinal cord was performed. Normal pyramidal cells in hippocampal CA1 area were harvested and histological grade was graded. The other 8 rats were subjected to Morris water maze test to detect spatial learning and memory function. Results The 400-mg PA seat was (5745 ± 1036) g, the TD seat was (6.87 ± 0.58) ms, the head of PA was (701 ± 309) g, and the head of TD was (1.00 ± 0.14) ms. ± 1167) g, TD was (11.08 ± 1.43) ms, the head of PA was (3383 ± 935) g and the head of TD was (1.32 ± 0.18) ms. There were significant differences between the two groups in the corresponding parameters (P <0.01). At 6 hours after injury, the gross anatomy of the rats showed no obvious abnormalities. However, the neurons in the brain and spinal cord under the light microscope changed acutely. The ultrastructure of capillaries and axons were also observed under electron microscope in 800mg group. Hippocampal CA1 histological damage classification: 800mg group> 400mg group> control group; neuron density: 800mg group <400mg group