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作 者:罗晨芳[1] 刘德昭[1] 张瑷兰[1] 池信锦[1]
机构地区:[1]中山大学附属第三医院麻醉科,广东广州510630
出 处:《中山大学学报(医学科学版)》2013年第1期65-69,共5页Journal of Sun Yat-Sen University:Medical Sciences
基 金:广东省科技计划项目(2011B031800058);广东省卫生厅基金项目(A2009197)
摘 要:【目的】观察一氧化氮(NO)吸入对肝移植急性肺损伤大鼠肺组织诱导型NO合酶(iNOS)、白细胞介素-1β(IL-1β)、白细胞介素-6(IL-6)水平的影响与意义。【方法】选用SD大鼠24只,按随机数字表法分为对照组(C组)、自体原位肝移植组(M组)和NO吸入组(T组),每组8只。对照组开腹游离肝叶后即关腹,后两组行大鼠自体原位肝移植。对照组及自体原位肝移植组术后于室内吸空气,NO吸入组术后即放入特制的密封盒内(NO体积分数为20×10-6)。手术结束后8 h行肺脏病理检查,测定肺组织干湿质量比(W/D),并检测iNOS、IL-1β、IL-6水平。【结果】①C组肺组织结构基本正常,M组肺组织炎症损伤明显,T组肺组织炎症损伤较M组明显减轻。②M组肺组织W/D明显高于对照组,T组则低于M组,但仍高于对照组。③M组iNOS活性及蛋白表达、IL-1β、IL-6水平较C组明显升高,T组则较M组降低,但仍高于C组。【结论】肝移植术后NO吸入可抑制肺组织iNOS活性及蛋白表达,降低IL-1β、IL-6水平,肺组织病理损伤减轻,干湿质量比下降。[Objective] To study the effects of inhaled nitric oxide (iNO) on iNOS (inducible nitric oxide synthase), IL-1β (interleukin-lβ) and IL-6 (interleukin-6) of lung tissue in rats with acute lung injury post liver transplantation. [Methods] Twenty- four SD rats were randomly divided into three grou ps: 1) a sham-operation control group (C group), the abdomen was only opened and then closed besides the liver lobes were isolated, without NO inhalation. 2) an autologous OLT group (M group), received autologous OLT, without NO inhalation. 3) an iNO group (T group), received autologous OLT, with 20 x 10-6 NO inhalation. The lung was removed at 8 h after operation and pathological changes were observed. The concentration of iNOS, IL-1β, and IL-6 in lung tissue were respectively examined in each group, lung wet -to- dry weight ratio (W/D) were also measured. [Results] (1)The lung pathological section of C group was normal, but in M group it showed inflammatory injury. The lung inflammatory injury was improved in T group. (2) Lung dry-to-wet weight ratio in M group was higher than in C group. It decreased in T group, but still higher than in C group. (3) The levels of iNOS, IL-1 β, and IL-6 in M group were higher than in C group. All decreased in T group, but still higher than in C group. The expression of iNOS showed the same change. [Conclusion] Inhaled NO after autologous OLT inhibits the activity of iNOS in lung, decreases the production of IL-1βand IL-6, attenuates pathological changes, and decreased lung wet -to- dry weight ratio.
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