大鼠心肌缺血再灌注损伤中肿瘤坏死因子的实验研究  

Tumor Necrosis Factor in Myocardial Ischemia Reperfusion Injury in Rats

作　　者：徐世安[1] 朱兵[1] 陈晓慨[1] 王占明[1] 

机构地区：[1]中国医科大学附属第二医院心脏外科,辽宁沈阳110004

出　　处：《中国医科大学学报》2003年第6期488-489,492,共3页Journal of China Medical University

基　　金：辽宁省科技攻关项目 (0 0 2 2 5 0 0 1)

摘　　要：目的 :探讨肿瘤坏死因子 (TNF)在心肌缺血再灌注损伤中的作用机制。方法 :应用大鼠Langendorff离体心脏灌注模型 ,通过酶联免疫法测定心肌组织TNF含量 ,原位杂交检测TNFmRNA的表达情况。结果 :对照组心肌组织中可以检测到一定含量的TNF ,但实验组心肌组织中的TNF水平较对照组明显升高 (P <0 .0 5 )。对照组心肌组织中没有TNFmRNA表达 ,染色呈阴性 ;实验组心肌组织中的TNFmRNA表达明显 ,染色呈强阳性或极强阳性 ,并将阳性表达的细胞定位于心肌细胞。结论 :TNF是在离体的、缺血心脏中产生的 ;TNF表达主要定位于心肌细胞 ,在心肌缺血再灌注损伤过程中 。Objective: Our aim was to study the mechanism of tumor necrosis factor (TNF) in ischemia reperfusion injury. Methods:We used ELISA to detect the level of myocardial TNF and in situ hybridization to visualize the presence and localization of TNF mRNA in isolated Langendorff heart models of rats. Results:In the control group, the myocardial TNF can be detected, but the level of myocardial TNF was higher in the experimental group underwent ischemia/reperfusion (P<0.05). The expression of TNF mRNA could not be detected in the hearts of the control group. There was obvious expression of TNF mRNA in the hearts in the experimental group. In situ hybridization showed that TNF was localized in cardiac myocytes. Conclusion:The TNF was produced in isolated ischemic heart,and cardiac myocytes was the major source of TNF which usually cause postischemic myocardial dysfunction.

关 键 词：缺血再灌注损伤 肿瘤坏死因子 

分 类 号：R364.1[医药卫生—病理学]