摘要
目的 明确耗竭补体对心肌缺血再灌注的保护作用。方法 12只小猪随机分为对照组和眼镜蛇毒因子 (CVF)组 ,CVF组在结扎冠状动脉前 6h按 2 0U/kg注射CVF以耗竭补体。开胸结扎小猪左冠状动脉前降支 6 0min ,然后松扎 5h。测定血流动力学、梗死面积、心肌组织髓过氧化物酶(MPO)等指标 ,并作免疫组织化学检查。结果 (1)血流动力学 :两组左室内压上升最大速度 (+dp/dtmax)在心肌缺血期间均有明显下降 ,再灌注 5h后对照组回升至 (32 6± 42 )kPa/s,而CVF组回升达(4 18± 41)kPa/s (P <0 .0 5 ) ;(2 )心肌梗死面积 (坏死区占左心室重量百分比 ) :对照组为 (13.2±4.0 ) % ,CVF组仅为 (7.6± 2 .8) % (P <0 .0 5 ) ;(3)MPO活性 (U/g) :对照组坏死区为 2 .6 8± 0 .15 ,而CVF组为 1.2 7± 0 .14(P <0 .0 1) ;(4 )免疫组化染色 :对照组坏死区心肌组织有明显C1q、C3、C5b 9的沉积。结论 CVF耗竭补体对小猪心肌缺血再灌注有显著心肌保护作用 。
Objective To investigate the protective effect of complement depletion on myocardial ischemia and reperfusion(MI/R). Methods Twelve baby pigs were randomized into the control and CVF groups. The latter received an injection of 20 U/kg cobra venom factor(CVF) 6 h before MI/R. Myocardial ischemia was induced by ligating the left anterior descending (LAD) coronary artery for 60 min. The ligature was then untied to bring about reperfusion for 5 h. The hemodynamic parameters including the myocardial infarct area and myeloperoxidase (MPO) activity were measured, and immunohistochemical analysis was also done. Results (1) Despite the same drop during the LAD occlusion in both groups, +dp/dt max (kPa/s) returned much more in the CVF group than in the control group after 5 h of reperfusion (418±41 vs 326±42, P <0.05). (2) The area of myocardial necrosis, expressed as a percent of the left ventricular mass, was smaller in the CVF group than that in the control group [(7.6±2.8)% vs (13.2±4.0)%, P <0.05]. (3) Myocardial MPO activity(U/g) in the necrotic zone in the CVF group was significantly lower when compared with the control group (1.27±0.14 vs 2.68±0.15, P < 0.01). (4) Immunohistochemistry analysis demonstrated extensive immunolocalizations of Clq, C3 and C5b 9 in the necrotic myocardium in the control group, whease these complement deposits were less extensive in the CVF group. Conclusions Conmplement depletion with CVF can protect myocardium from ischemia and reperfusion injury. The mechanism of this cardioprotective effect may be related to the inhibition of PMN activation.
出处
《中华心血管病杂志》
CAS
CSCD
北大核心
2001年第6期365-368,I001,共5页
Chinese Journal of Cardiology
基金
卫生部科学研究基金资助 (96 1 115 )
