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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GSNO50μg/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、48hCBF和血浆神经元特异性烯醇化酶(neuron-specific 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1h CBF较伤前明显降低,达最低值(P<0.01),伤后24h仍低于伤前(P<0.01)。舱外组伤后1h CBF降低达最低值(P<0.01),伤后12h恢复至伤前水平。2组CBF在伤后1、6、12、24h存在显著差异(P<0.01)。舱内组经GSNO治疗后CBF明显升高,在伤后1、6、12、24h存在显著差异(P<0.01)。舱内组血浆NSE浓度及脑水肿指数均在伤后6h达峰值,显著高于对照组(P<0.01),伤后48h仍高于对照组(P<0.05)。舱外组则在伤后12h达峰值,显著高于对照组(P<0.01),伤后48h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(P<0.05)。舱内组经GSNO治疗后血浆NSE浓度及脑水肿指数明显降低(P<0.01)。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 study the changes and significance of cerebral blood flow (CBF) in rats after explosion in cabin. Methods 160 Sprague-Dawley rats were randomly divided into intranasal group, extra-group group and S-Nitrosoglutathione (GSNO) group, 48 rats in each group. DDNP paper explosion was used to simulate Explosion of armored cabins and open space to establish a model of brain injury. The GSNO treatment group was intraperitoneally injected with GSNO 50 μg / kg immediately after intracavitary injury. Another 16 normal control group (LDF) and double antibody sandwich method (ELISA) were used to detect the specific expression of CBF and plasma neurons at 1, 6, 12, 24 and 48 h after injury The neuron-specific enolase (NSE) concentration was measured and brain edema index was taken for pathological observation. Results The level of CBF in group I was significantly lower than that in the 1 hour after injury (P <0.01). The level of CBF in group I was lower than that before injury (P <0.01). At 1 hour after injury, the CBF decreased to the lowest level (P <0.01), and recovered to the pre-injury level 12 hours after injury. There were significant differences between the two groups at 1, 6, 12 and 24 hours after injury (P <0.01). After intragastric administration of GSNO, CBF was significantly increased, with significant differences at 1, 6, 12 and 24 hours after injury (P <0.01). The concentration of NSE and the index of cerebral edema both reached the peak at 6h after injury, significantly higher than that of the control group (P <0.01), and still higher than that of the control group 48h after injury (P <0.05). The extravasation group peaked at 12 hours after injury, significantly higher than that in the control group (P <0.01), and recovered to the pre-injury level 48 hours after the injury. The concentration of NSE in plasma and the index of cerebral edema were higher in cabin group than those in cabin group (P <0.05). After intragastric administration of GSNO, the plasma NSE concentration and cerebral edema index were significantly decreased (P <0.01). Pathological observation of intracavitary group showed obvious changes of brain edema, manifested as vascular endothelial cell swelling, neuronal shrinkage, degeneration, necrosis, the surrounding space was significantly wider and other changes. Extravascular group and treatment group were only a small amount of nerve cell degeneration and necrosis. Conclusion The decrease of cerebral blood flow in exploded rats exposed to open environment is more serious and lasts longer. The decline of cerebral blood flow may be involved in secondary brain damage after brain injury in rats.