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纸质出版:2010
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许明伟,许民辉,赖西南,王丽丽,张子焕,崔红.舱室内爆炸致大鼠脑血流量改变及其意义[J].陆军军医大学学报(原第三军医大学学报),2010,32(18):1962-1966.
Xu Mingwei,Xu Minhui,Lai Xinan,Wang Lili,Zhang Zihuan,Cui Hong.Changes in cerebral blood flow and significance in rats after blast brain injury in enclosed space[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(18):1962-1966.
许明伟,许民辉,赖西南,王丽丽,张子焕,崔红.舱室内爆炸致大鼠脑血流量改变及其意义[J].陆军军医大学学报(原第三军医大学学报),2010,32(18):1962-1966. DOI:
Xu Mingwei,Xu Minhui,Lai Xinan,Wang Lili,Zhang Zihuan,Cui Hong.Changes in cerebral blood flow and significance in rats after blast brain injury in enclosed space[J].J Amry Med Univ (J Third Mil Med Univ),2010,32(18):1962-1966. DOI:
目的 研究舱室内爆炸致伤后大鼠脑血流量(cerebral blood flow,CBF)变化及其意义。 方法 160只SD大鼠完全随机分为舱内组、舱外组
S-亚硝基谷胱甘肽(S-Nitrosoglutathione
GSNO)治疗组,各48只
采用DDNP纸质点爆源在模拟装甲舱室和舱外开阔地爆炸建立颅脑爆炸伤模型。GSNO治疗组为舱室内致伤后立即给予GSNO 50 μg/kg腹腔内注射。另设正常对照组(16只);采用激光多普勒血流仪(LDF)和双抗体夹心法(ELISA)检测伤前、伤后1、6、12、24、48 h CBF和血浆神经元特异性烯醇化酶(neuronspecific enolase, NSE)浓度,取脑组织测脑水肿指数并行病理学观察。 结果 舱内组伤后1 h CBF较伤前明显降低,达最低值(P0.01),伤后24 h 仍低于伤前(P0.01)。舱外组伤后1 h CBF降低达最低值(P0.01),伤后12 h恢复至伤前水平。2组CBF在伤后1、6、12、24 h存在显著差异(P0.01)。舱内组经GSNO 治疗后CBF明显升高,在伤后1、6、12、24 h存在显著差异(P0.01)。舱内组血浆NSE浓度及脑水肿指数均在伤后6 h 达峰值,显著高于对照组(P0.01),伤后48 h仍高于对照组(P0.05)。舱外组则在伤后12 h达峰值,显著高于对照组(P0.01),伤后48 h恢复致伤前水平。舱内组血浆NSE浓度及脑水肿指数均较舱外组升高显著(P0.05)。舱内组经GSNO治疗后血浆NSE浓度及脑水肿指数明显降低(P0.01)。病理学观察舱内组可见明显脑水肿改变
表现为血管内皮细胞肿胀,神经元皱缩、变性、坏死、周围间隙明显增宽等改变。舱外组及治疗组均仅见少量神经细胞变性、坏死。 结论 舱室内爆炸较开阔环境地爆炸大鼠脑血流量下降程度重、持续时间长。脑血流量的下降可能参与了大鼠颅脑爆炸伤后的继发性脑损害。
Objective To investigate the dynamic changes of cerebral blood flow in rats with brain injury caused by explosion. Methods A total of 160 male rats were divided randomly into enclosure group (n=48)
open-field group (n=48) and S-Nitrosoglutathione (GSNO) therapy group (n=48)
and subjected to explosion with instantaneous electric detonator. Sixteen uninjured rats served as normal control. Before and in 1
6
12
24 and 48 h after injury
cerebral blood flow of were measured by laser Doppler flowmetry (LDF)
plasma level of neuron-specific enolase (NSE) was measured by ELISA
and brain tissues were analyzed by wet-dry weight measurements and microscopy after HE staining. Results The CBF was significantly reduced to the lowest value in 1 h after injury in enclosure group (P0.01). The value was still lower than pre-injury in 24 h after injury (P0.01). The CBF of open field group was also reduced to the lowest value at 1 h after injury (P0.01)
but it recovered to pre-injury level at 12 h after injury. The CBF in 2 group at 1
6
12 and 24 h after injury were significantly different (P0.01). The CBF of enclosure group was significantly elevated after GSNO intervention. NSE concentration and brain water content of enclosure group were elevated to the highest value at 6 h after injury (P0.01)
and were still higher than control group at 48 h after injury (P0.05). But in open field group
the value were elevated to highest at 12 h after injury(P0.01)
and recovered to the level of control group at 48 h after injury. The value of GSNO therapy group was significantly lower than enclosure group (P0.01). The pathological changes of enclosure group showed obvious brain edema
swelling of endothelial cells
neuron shrinkage
degeneration
necrosis
significantly widened gap around neuron and so on. But the GSNO therapy group only showed neuron necrosis. Conclusion The reduction of cerebral blood flow sustains longer and stronger in rats in enclosed space than that in open field. Decreased cerebral blood flow may be involved in the secondary brain injury after explosive brain injury.
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