心肌缺血再灌注中TNF动态变化及药物干预

目的探讨肿瘤坏死因子(TNF)、髓过氧化物酶(MPO)在心肌缺血再灌注(MI/R)中的动态变化的临床意义及卡托普利的干预作用。方法将实验兔54只分为MI/R组、卡托普利治疗组及假手术对照组,分别测缺血前、缺血0.5h,再灌注0.5、1.5、6h5个时相点外周血TNF,以及后4个时相点心肌组织TNF、MPO含量,对照组心肌指标只检测最后一个时相点。结果再灌注0.5h外周血TNF即开始升高(P<0.05),再灌注6h更高(P<0.01),心肌组织TNF、MPO含量则于再灌注1.5h升高并持续至再灌注6h,卡托普利干预后上述指标均有明显改善。结论TNF参与再灌注损伤,是再灌注后导致内皮功能紊乱的重要因素之一。卡托普利通过保护内皮,减少致伤因素而减轻再灌注损伤。

Dynamic changes of TNF and Captopril Intervention during myocardial ischemic reperfusion

Objective To study the dynamic changes of tumor necrosis factor(TNF ),myeloperoxidase(MPO) during myocardial ischemic reperfusion(MI/R) and therapeu tic effect of captopril. Methods All 54 rabbits were divided into 3 groups ran dom MI/R group(A), captopril group(B) and sham-operated group(C).Serum TNF, T NF and MPO of myocardial tissue were measured before ligation, 0.5h after ischem ia and 0.5,1.5 and 6 hours after reperfusion(n=6,in each time-point). Results C omparing to group C serum TNF increased in 0.5h(P<0.05) and higher in 6h after r eperfusion (P<0.01).Tissue TNF and MPO increased in 1.5h after reperfusion(P<0.0 1); Captopril decreased the indices remarkedly. Conclusions TNF could play an i mportant role during MI/R. Captopril can decrease myocardial reperfusion injury through protecting endothelial cell from damage.