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心肌梗塞再灌注中血浆白细胞介素6的动态变化和其单克隆抗体的保护效应 |
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on were not different between Group A and Group B, but markedly higher than those of the normal controls (P<0.01), and lasted to 24 hours after AMI. Plasma IL-6 level and CD11b expression were significantly higher in Group A than in Group B at 1 and 4.5 hours after reperfusion (P<0.01, P<0.01). (2) In the rabbit model, the changes of plasma IL-6 level and CD11b expression were similar to those of AMI patients. In addition, accumulation of neutrophils and MPO activity significantly increased in ischemic cardiac tissue. IL-6 release was correlated with CD11b expression and MPO activity (r=0.924 and 0.622, respectively, P<0.01). Reperfusion (4 hrs) following ischemia (1.5 hrs) significantly increased size of myocardial infarct compared with ischemia (1.5hrs) alone ［(43.8±3.9) % vs (38.7±3.5) %, P<0.05］, whereas it markedly reduced infarct size compared with ischemia (5.5 hrs) ［(43.8±3.9) % vs (52.9±4.8) %, P<0.05］. McAb-IL6 treated rabbits showed less CD11b expression, MPO activity and infarction size ［(27.5±3) % vs (43.8±3.9) %, P<0.01］. Conclusion IL-6 plays a critical role in myocardial ischemia postreperfusion inflammatory injury. Monitoring the changes of plasma IL-6 and CD11b would help to recognize myocardial ischemia reperfusion injury. McAb IL-6 might be useful clinically at reducing myocardial ischemia postreperfusion inflammatory injury.
【Key words】 interleukin-6 monoclonal antibody myocardial infarction reperfusion injury
心肌缺血最根本的治疗措施是恢复血供，但重建血供本身将在一定程度上引起组织的进一步损伤［1］。心肌缺血再灌注的部分损伤被认为与中性粒细胞和血管内皮细胞及心肌细胞的相互作用有关。同时，细胞因子起着调节和修饰作用［2］。有研究表明，中性粒细胞的消耗可减少心肌缺血再灌注损伤。实验动物的心肌缺血再灌注区有白细胞介素6(IL-6) mRNA的表达，其表达高峰在再灌注3小时［3］。
本研究观察了急性心肌梗塞(AMI)患者和兔的AMI模型在心肌缺血再灌注期间IL-6的动态演变及其单克隆抗体(McAb-IL6)对心肌缺血再灌注损伤的效应。
资料与方法
一、临床资料
1.AMI组：符合WHO诊断标准的我院CCU住院患者28例，于发病平均(6±4.5)小时接受了链激酶(SK)或重组组织型纤溶酶原激活剂(t-PA)静脉溶栓治疗。28例中3例溶栓后90分钟行冠状动脉造影，余25例以临床指标判定血管再通［4］。(1)相关血管再通组13例，平均年上一页 [1] [2] [3] 下一页
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