缺血后处理对大鼠肠缺血再灌注致肺脂质过氧化损伤的保护作用

Protective effect of ischemic postconditioning on lipid peroxidation of lung following intestinal ischemia reperfusion in rats

目的研究缺血后处理(I-post C)对大鼠肠缺血/再灌注(I/R)致肺脂质过氧化损伤的保护作用。方法 32只健康雄性Wistar大鼠随机分为假手术(Sham)组、I/R组、肠缺血后处理(II-post C)组和肢体缺血后处理(LI-post C)组,以无创动脉夹夹闭肠系膜上动脉45 min,再灌注2 h建立肠I/R模型,采集动脉血进行血气分析,测定肺系数判定组织水肿情况,光镜下观察肺组织病理学改变,试剂盒测定血浆和肺组织超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量。结果与I/R组比较,II-post C组和LI-post C组PaO2升高而PaCO2降低(P<0.05),肺系数减小(P<0.01)且肺组织病理变化减轻;II-post C和LI-post C均可抑制肠I/R所致的血浆和肺组织SOD活性降低和MDA含量升高(P<0.05或P<0.01)。结论缺血后处理可减轻肠I/R大鼠肺损伤,其机制与抑制脂质过氧化反应有关。

Objective： To investigate the protective effect of ischemic postconditioning（I-post C） on lipid peroxidation of lung following intestinal ischemia reperfusion（I/R） in rats.Methods： Thirty-two male Wistar rats were randomly divided into sham,I/R,intestinal ischemic postconditioning（II-post C） and limb ischemic postconditioning（LI-post C） groups.Model of intestinal I/R injury was made by clamping super mesenteric artery for 45 min followed by 120 min of reperfusion in rats.At the end of the experiment,the changes of arterial blood gas level and lung index were measured and the morphological changes of lung tissue were observed through light microscope.Superoxide dismutase（SOD） activity and malondialehyde（MDA） content in plasma and lung tissue were detected.Results： II-post C and LI-post C improved the lung respiratory function,charactered by the increase of PaO2 and decrease of PaCO2（P0.05 vs I/R group）.The lung index was decreased（P0.01）,and the pathologic lesion of lung tissue was alleviated significantly by II-post C and LI-post C in comparison with those in I/R group.In addition,both II-post C and LI-post C markedly inhibited the decrease of SOD activity and increase of MDA content in plasma and lung tissue（P0.05 or P0.01） induced by intestinal I/R.Conclusion： I-post C attenuates lung injury induced by intestinal ischemia reperfusion in rats,which is related to the inhibition of lipid peroxidation reaction.