摘要
目的探讨重症急性胰腺炎(SAP)引起急性肺损伤(ALI)的机制.方法 48只实验组大鼠注射40g/L(4%)牛磺胆酸钠制作SAP模型.实验组及对照组(48只)大鼠分别在1、3、5、7、9、12h点剖杀,取胰腺及肺组织行病理观察、微血管通透性及MPO活性测定;RT-PCR法检测胰腺及肺组织中细胞间黏附分子(ICAM-1)、肿瘤坏死因子(TNF-α)基因表达.结果制模后胰腺及肺损伤逐渐加重,胰腺及肺髓过氧化物酶(MPO)活性及微血管通透性逐渐升高;胰腺TNF-α、ICAM-1基因表达均在1h明显升高,至7h达到峰值;肺组织TNF-α、ICAM-1基因表达则在1h后逐渐上升,至9～12h达到峰值.结论 SAP引起ALI过程中存在明显的时间窗口,该窗口内的早期预防性保护可能利于防止ALI的发生.
Objective To study the pathogenesis of acute lung injury in severe acute pancreatitis （SAP）. Methods To induce SAP model, 48 rats were treated with 4% sodium taurocholate. SAP and control rats were sacrificed at 1, 3, 5, 7, 9 and 12 hours. Pancreas and lung tissue were obtained for pathological study, microvascular permeability and myeloperocidase （MPO） examination. Gene expression of tumor necrosis factor （TNF-α ） and intercellular adhesion molecule （ICAM-1） in pancreas and lung tissue was detected by RT-PCR. Results After SAP model was established, the injured degree of the pancreas and the lung increased gradually, accompanied with gradual increase of MPO activity and microvascular permeability. Gene expression of TNF- α and ICAM-1 in pancreas increased at 1 hour and reached peak at 7 hours. Relatively, their gene expression in the lung only increased slightly at 1 hour and reach peak at 9-12 hours gradually. Conclusion There is an obvious time window of injury between pancreas and lung in SAP, and earlier protection is beneficial to prevent the occurrence of acute lung injury.
出处
《西安交通大学学报（医学版）》
CAS
CSCD
北大核心
2005年第4期371-373,共3页
Journal of Xi’an Jiaotong University（Medical Sciences）
基金
国家自然科学基金项目(No.30371398)
西安交通大学科学研究基金资助项目(No.Y100.573003)
关键词
机制
重症急性胰腺炎
急性肺损伤
TNF-Α
细胞间黏附分子
pathogenesis
severe acute pancreatitis
acute lung injury
tumor necrosis factor
intercellular adhesion molecule
