CD59对补体介导的心肌缺血损伤的保护作用

Protective effect of CD59 on the myocardial ischemic damage mediated by complements

目的 探讨CD5 9对补体介导的心肌缺血损伤的保护作用。方法 30只豚鼠离体工作心脏随机分为空白对照组 (A组 )、补体激活组 (B组 )和CD5 9干预组 (C组 ) ,分别接受 3%灭活人血浆 +酵母多糖、3%人血浆 +酵母多糖和CD5 9+3%人血浆 +酵母多糖 3种处理 ,记录各组处理前及处理后 15、30、45和 6 0min的心外膜心电图、心输出量(CO)、左心室最大内压 (LVPmax)和左心室内压最大上升速率 (dp/dtmax) ,并在实验结束时取左心室心肌组织进行免疫组化检查 ,观察有无C5b 9、C3a在心肌组织沉积。结果 B组在接受处理后心外膜心电图出现ST段抬高 ,心率增加 ,CO、LVPmax和dp/dtmax均下降 ,这些变化以处理后 45min最明显 ,A组、C组上述指标处理前后无明显变化。免疫组化检查 :B组可见C5b 9、C3a沉积 ,C组见C3a沉积 ,A组未见C3a和C5b 9沉积。结论 激活补体可直接引起豚鼠工作心脏心肌缺血损伤 ;CD5

Objective To evaluate the protective effect of CD59 on the myocardial ischemic damage mediated by complements.Methods Isolated guinea pig working hearts were perfused with 3% heat inactivated human plasma and zymosan in group A (control),3% normal human plasma and zymosan in group B and 3% normal human plasma and CD59 and zymosan in group C,respectively.Epicardial electrocardiogram (ECG),cardiac output (CO),maximum left ventricular developed pressure (LVP max ),maximum left ventricular pressure rise rate (dp/dt max ) and heart rate(HR) were recorded before and after 15,30,45 and 60 minutes of perfusion.After the experiment,immunohistochemical examination of left ventricular myocardium was performed to examine the deposition of C3a and C5b 9 in the myocardium. Results Elevation of ST segment,increased HR and decrease in CO,LVP max and dp/dt max were seen in group B after perfusion and were most prominent at 45 minutes of perfusion.No apparent change in all above parameters was seen in group A and group C before and after perfusion.Immunohistochemical examination showed the deposition of C3a and C5b 9 in the myocardium in group B,C3a in group C and no deposition of C3a or C5b 9 in group A.Conclusion Activated human complements directly induce myocardial ischemic damage of isolated guinea pig working hearts,which can be prevented by CD59.