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作 者:刘家传 孙文江 张永明 杨艳艳 汤宏 李兵仓[2] 张良潮[2]
机构地区:[1]解放军第一0五医院神经外科,合肥230031 [2]第三军医大学附属大坪医院野战外科研究所
出 处:《中华航海医学与高气压医学杂志》2012年第3期163-166,共4页Chinese Journal of Nautical Medicine and Hyperbaric Medicine
基 金:南京军区联勤部卫生部“十一五”重点基金项目(06219);南京军区医学科技创新课题(092009)
摘 要:目的通过研究高压氧(hyperaricoxygen,HBO)暴露对兔脑爆炸伤后脑组织水通道蛋白4(aquapodins-4,AQP-4)的表达及血液灌注的影响,探讨爆炸伤后脑水肿的形成机制。方法150只新西兰大白兔采用数字表法随机分为对照组、高压氧治疗组(HBO组)和非治疗组。HBO组与非治疗组用纸雷管爆炸制作兔脑爆炸伤模型,随后分别随机分为伤后lh、6h、12h、24h、72h、7d、14d7个亚组,每亚组10只,对照组10只。采用RT-PCR法测定兔脑组织中AQP-4mRNA的表达,磁共振灌注成像(perfusionweightedimaging,PWI)检测伤后不同时间点伤后脑组织血液灌注情况。结果AQP-4mRNA在伤后1h表达开始上调,3d达峰值,7d后缓慢下调。经HBO早期治疗,在6h后各时间点AQP-4mRNA表达均明显下调(P〈0.05)。如伤后6h,非治疗组AQP-4mRNA相对量为0.5184-0.088,HBO组为0.327±0.027。经PWI检测,非治疗组伤后早期灌注明显下降,12h后灌注逐渐上升,并保持一定灌注量(接近对照组)持续2周;伤后早期(1-6h)治疗组灌注下降更为明显。结论HBO早期治疗可有效提高兔爆炸伤后脑组织血氧分压,增加血氧含量,缓解脑组织缺氧引起的继发性脑水肿。Objective Mechanism of cerebral edema following blast injury in rabbits through the study of the expression of aquapodins- 4 ( AQP- 4 ) introduced by HBO, and perfusion as well, after cerebral blast injury. Methods One hundred and fifty New Zealand rabbits were randomly divided into the treatment group, the non-treatment group and the control group ( l0 animals ). The animal model of cerebral blast injury was developed by using paper detonator. The treatment and the non-treatment groups were randomly divided into the 1 h, 6 h, 12 h, 24 h, 72 h, 7 d and 14 d sub-groups, each consisting of 10 animals. The expression of AQP- 4 mRNA was measured with RT-PCR, and the perfusion of the brain tissue was detected with perfusion weighted imaging (PWI) at each time points, following cerebral injury. Results The expression of AQP-4 mRNA began to increase 1 h after injury, reached peak in 72 h, and then decreased at day 7. Following initial HBO treatment, the expression of AQP- 4 mRNA significantly decreased at various time points after 6 hours ( P 〈 O. 05 ). PWI test indicated that blood perfusion for the non-treatment group significantly decreased in the initial stage of injury, however, 12 h after injury perfusion gradually increased, and the amount of perfusion ( close to the control group) was maintained for 2 weeks. For the treatment group, perfusion decreased more significantly in the early stages of injury ( 1-6 b). Conclusions Early HBO therapy could enhance the partial pressure of oxygen in the affected brain tissue, increase blood oxygen content and alleviate secondary cerebral edema induced by cerebral ischemia.
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