摘要
目的 :研究SMT对心脏缺血 再灌注损伤 (IRI)心肌超微结构的影响。方法 :SD大鼠 18只 ,体重 32 0~ 380g ,随机分为三组 :①缺血 再灌注组 (IR) :夹闭冠状动脉左前降支 6 0min ,松夹 2 0min ;②缺血 再灌注 +SMT组(SMT) :再灌注前 5min ,股静脉注射iNOS抑制剂S methylisothioureasulfate(SMT 5mg/kgw ) ,余同IR组 ;③对照组 (C) :暴露心脏后 ,不做任何处理 ,观察 80min。测量Ⅱ导联心电图 ,测定心肌NO2 -+NO3-、实验前后血清NO2 -+NO3-含量 ,心肌组织透射电镜检查。结果 :IR组血清NO2 -+NO3-较实验前明显增高 (P <0 .0 1) ,心肌组织NO2 -+NO3-高于C组 (P <0 .0 5 )。电镜观察 ,心肌纤维过度收缩 ,线粒体肿胀、嵴断裂 ,排列紊乱、空泡形成。SMT组实验后血清NO2 -+NO3-较实验前降低 (P <0 .0 5 ) ,心肌组织NO2 -+NO3-接近C组 (P >0 .0 5 )、低于IR组 (P <0 .0 5 )。电镜下 ,心肌超微结构损伤明显改善。线粒体群集 ,电子密度增高 ,嵴密集、排列整齐 ,肿胀及空泡明显减轻。结论
Aim: To Investigate the myocardial ultrastructure effects of SMT on the ischemia reperfusion injury (IRI) in the rat heart. Methods: Eighteen Spraqua Dawley rats were randomly divided into three groups: ischemia reperfusion group (IR), subjected to 60 min of o cclusion and 20 min of reperfusion of the anterior descending branch of left coronary artery; IR+SMT group (SMT) , given the selective iNOS inhibitor S methylisothiourea sulfate (SMT, 5mg/kg, Ⅳ) before reperfusion; control group (C), didn't occlude coronary artery after exposing heart and observed 80 min.Electrocardiogram (ECG) was recorded. Nitrite and nitrate content were measured in myocardium and blood serum. The changes of myocardial ultrastructure were observed with electron microscope. Results: Ischemia reperfusion induced ST segment elevation and T waves inversion or tallness in ECG, damaged myocardial ultrastructure, increased nitrite and nitrate content in myocardium and blood serum after IR compared with before IR( P <0.01). Administration of SMT improved the changes of ECG and the injury of myocardial ultrastructure. Nitrite and nitrate content of myocardium were lower than IR group ( P <0.05). The change of nitrite and nitrate level of blood serum in SMT group was nearly in C group. Conclusion: SMT can prevent myocardium injury from reperfusion following ischemia.
出处
《中国应用生理学杂志》
CAS
CSCD
2000年第4期314-317,共4页
Chinese Journal of Applied Physiology
基金
广东省科委攻关资助项目!(980 2 )
关键词
心脏
缺血-再灌注损伤
一氧化氮合酶
超微结构
myocardium
ischemia reperfusion injury
nitric oxide synthase
ultrastructure.