摘要
目的 观察大鼠肠缺血 再灌注后肺组织致炎因子和ICAM 1表达的特点及其与中性粒细胞在肺中扣押的关系。方法 采用肠系膜上动脉夹闭 松夹闭的方法复制大鼠肠缺血 再灌注模型。在不同的时相检测血浆血管紧张素转换酶 (ACE)活性 ,肺组织TNF ,IL 6 ,ICAM 1mRNA及蛋白表达水平和MPO活性的变化。结果 肠缺血和再灌注后早期肺组织TNF ,IL 6 ,mRNA和蛋白水平无明显改变 ,但再灌注 6h后均大幅度升高 ;血浆ACE活性、肺ICAM 1表达及MPO活性变化趋势与其一致。结论 肠缺血 再灌注引起肺组织炎症介质和黏附分子表达上调 ,由此介导PMN在肺中扣押 。
Objective To investigate the expression of inflammatory mediators and ICAM-1,and to explore their relation to the sequestration of polymorphonuclear cells in the lung tissue after gut ischemia and reperfusion.Methods The superior mesenteric artery was occluded and then released to produce the the model of gut ischemia-reperfusion in rats.At different time points after ischemia and reperfusion,the plasma angiotensin converting enzyme(ACE)activity was assayed,and the expressions of TNF-α,IL-6,ICAM-1,and MPO activities in lung were measured.Results During gut ischemia and early reperfusion,the expression levels of TNF_α and IL-6 in lung did not change significantly,but at 6 h after reperfusion,TNF-α expression increased significantly,accompanied by increasement of plasma ACE activity,an up-regulation of ICAM-1expression,and enhanced MPO activity in the lung.Conclusion Gut ishcemia-reperfusion can up-regulate the expression of inflammatory mediators and ICAM-1,which lead to the PMN cells sequestration in the lung.This may cause lung injury.
出处
《中华急诊医学杂志》
CAS
CSCD
2003年第10期670-672,T002,共4页
Chinese Journal of Emergency Medicine
基金
全军"九五"重点科研基金资助 (0 1LO81)
