高氧肺损伤;二异丙酚;活性氧;细胞结构;大鼠____

异丙酚对高氧肺损伤大鼠氧自由基、IL8及肺组织超微结构的影响

http://www.100md.com 《齐鲁医学杂志》 2007年第2期

高氧肺损伤;二异丙酚;活性氧;细胞结构;大鼠,,],高氧肺损伤;二异丙酚;活性氧;细胞结构;大鼠,1材料与方法,2结果,3讨论,参考文献]

     [摘要] 目的建立大鼠高氧肺损伤模型,观察异丙酚对高氧肺损伤的保护作用,并探讨其机制。方法选取SD大鼠72只,随机分为3组,每组24只。A组为空气对照组，B组为高浓度氧组(氧体积分数0.80～1.00)，C组为高浓度氧+异丙酚处理组。分别于实验第3、5、7小时每组取8只大鼠,检测血清及支气管肺泡灌洗液中超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSHPx)的活性、丙二醛(MDA)含量及白细胞介素8(IL8)浓度,同时电镜下观察各组大鼠肺组织超微结构变化。结果与A组、C组相比较，B组SOD、GSHPx的活性显著下降,MDA含量、IL8浓度显著上升(F=5.86～18.41,q＝3.15～7.17,P<0.01);与A组比较，C组SOD、GSHPx活性无明显变化，MDA含量及IL8浓度轻微上升，但无统计学差异。B组肺组织线粒体破坏，呈空泡样变,C组仅见线粒体轻微肿胀。结论异丙酚抑制氧自由基产生和炎性细胞因子的分泌,减轻肺组织超微结构的改变，对大鼠高氧肺损伤具有一定的保护作用。

    [关键词] 高氧肺损伤;二异丙酚;活性氧;细胞结构;大鼠

    INFLUENCE OF PROPOFOL ON OXYGENDERIVED FREE RADICALS, IL8 AND ULTRASTRUCTURE CHANGES OF RAT LUNG INDUCED BY HYPEROXIACHI MEIYING， PAN XIAOJUN， ZHAO YONG, et al (Department of Anesthesiology， Liaocheng Peoples Hospital, Liaocheng 252000, China)

    [ABSTRACT]ObjectiveTo establish an animal model of lung injury caused by hyperoxia and to observe the preventive effect of propofol against the lung injury in rats. MethodsSeventytwo healthy male SD rats were randomly divided into three groups: group A, normal control group; group B, hyperoxia group (80%-100% oxygen); and group C, propofol group (80%-100% oxygen+ propofol 8 mg/kg BW·h-1). Blood and bronchoalveolar lavage fluid (BALF) were taken at 3rd h, 5th h and 7th h of the experiment to check the activity of SOD and GSHPx and the levels of IL8 and MDA. Morphological changes of the lung tissue were observed electronmicroscopically. ResultsCompared with group A and group C, significant increase in the levels of IL8 and MDA and decrease in the activities of SOD and GSHPx were noted in group B (F=5.86-18.41,q＝3.15-7.17, P<0.01); compared with group A, the activity of SOD and GSHPx was not changed markedly, the levels of IL8 and MDA rised slightly but with no statistically significant. Mitochondria became vacuolated and deformed in group B, slightly swollen in group C. ConclusionPropofol protects the lung from damage caused by hyperoxia in rats by decreasing oxygenderived free radicals and IL8 as well as ultrastructural changes in lung tissuse. ......

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