黏附因子-1、IL-18在大鼠左心缺血再灌注诱导的急性肺损伤中的作用

目的:探讨白介素-18、黏附因子-1在左心缺血再灌注肺损伤中的作用及对呼吸功能的影响.方法:60只SD大鼠随机均分为实验组和对照组,实验组复制左心缺血再灌注肺损伤模型并与BL-420生物信号采集分析系统相联,对照组不做左冠状动脉的前降支结扎其余操作同实验组.比较缺血30min、再灌注30min、再灌注60min3个时间点两组大鼠肺组织白介素-18、黏附因子-1表达情况、外周血和支气管肺泡灌洗液中白介素-18水平、动脉血氧分压及呼吸曲线进行比较.结果:各时间点实验组大鼠肺组织白介素-18、黏附因子-1表达高于对照组;外周血和支气管肺泡灌洗液中白介素-18水平高于对照组;PaO2低于对照组;呼吸曲线的幅度、强度、持续时间均低于对照组,上述差异均具有统计学意义(P<0.05).结论:白介素-18激活黏附因子-1释放增多,吸引白细胞在肺循环发生黏附聚集释放反应,引起炎性细胞因子的进一步释放,导致肺炎症反应失衡,引起急性炎症损伤,致呼吸功能下降.

Effects of IL-18 and ICAM-1 on Respiratory Function in Rat with Acute Lung Injury Induced by Left Heart Ischemic Reperfusion

Objective:To study Effects of interleukin-18(IL-18) and inflammatory cell adhesion molecules-1(ICAM-1) on respiratory function in rat with acute lung injury induced by left heart ischemic reperfusion.Methods:60 rats were randomly divided into the experimental group(EG)and the control group(CG).The rats of EG group copied the model of left heart ischemia-reperfusion that was made through ligaturing and loosing the anterior descending branch.The rats of CG group didn`t copy the modle.These rats were sacrificed after 30 minutes after ligaturing(T1),30 min utes after loosing(T2) and 60 min utes atter loosing(T3) respectively,observed respiration curve and arterial partial pressure of oxygen with BL-420 computer system,measured the expression of IL-18 and ICAM-1 with Immunohistochemistry,measured the expression of IL-18 in peripheral blood and bronchial alveolarlavage fluid with Enzyme Linked Immunosorbent Assay methods.All results were recorded and comparatively analyzed.Result:The level of the expression of IL-18 and ICAM-1 were higher than CG group,the activity of myeloperoxidase in lung tissue of EG were stronger than CG group,the expression of IL-18 in peripheral blood and bronchial alveolarlavage fluid were higher than CG group,the arterial partial pressure of oxygen of EG were Lower than CG group,and the respiration curve of EG group were worse than CG group in range,standing and frequency.These differences were significant(P<0.001).Conclusion:ICAM-1 can be liberated with IL-18,causing leukocyte adhesiveness which can release more inflammatory cytokines,which can expand inflammatory cascade response,so they can cause acute lung injury and respiratory dysfunction.