炎性因子及补体成分在心肌梗死发病机制中的作用探讨  

Study of the role of inflammatory cytokines and complement in the pathophysiological process of acute myocardial infarction

作　　者：黄红莹[1] 惠学志[2] 尹学亮[2] 许国强[1] 

机构地区：[1]河南大学医学院病原生物学教研室,河南开封475001 [2]河南大学医学院第一附属医院

出　　处：《中国急救医学》2001年第5期261-262,共2页Chinese Journal of Critical Care Medicine

基　　金：河南省教育厅自然科学研究基金资助项目 !(973 2 0 0 44)

摘　　要：目的　探讨IL - 8、TNF -α及sC5b - 9在心肌梗死发病机制中的作用。方法　用双抗体夹心酶联免疫吸附法对 38例AMI患者及 40名健康人进行IL - 8、TNF -α及sC5b - 9测定。结果　AMI患者血清IL - 8、TNF -α及sC5b - 9含量明显升高 ,与健康人比较有显著性差异 (P <0 0 1) ;在AMI发病后第 7天 ,IL - 8、TNF -α及sC5b - 9水平逐渐下降 ,到第 2 8天上述变化仍未达到对照组水平。结论　IL - 8、TNF -α及sC5b - 9参与心肌缺血的形成 ,并与心肌坏死的范围成正相关。Objective To study the role of inflammatory cytokines and complement in the pathophysiological process of acute myocardial infarction(AMI).Methods By use of enzyme-linked immunosorbent assay (ELISA),changes serum interleukin-8、tumor necrosis factor-α and composition of complement activation(sC5b-9)levels were measured in 38 AMI and 40 healthy controls.Results The serum interleukin 8、tumor necrosis factor-α and composition of complement activation (sC5b-9)levels were higher in AMI than those in healthy controls ( P <0 01).The levels of cytokines and complement began to recover form 7 days after the AMI but they did not reach the normal level until 28 days after AMI.Conclusions The cytokines and complement participate in the pathophysiology of AMI.The levels of which are correlated with the severity of the disease.The use of anti-inflammatory may be a useful method for treatment of AMI. [

关 键 词：心肌梗塞 血清 白细胞介素-8 肿瘤坏死因子Α 补体 ELISA 

分 类 号：R542.22[医药卫生—心血管疾病] R392.3[医药卫生—内科学]