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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 :SMT对IRI的心肌超微结构有保护作用
Objective: To investigate the effect of SMT on cardiac ultrastructure of myocardial ischemia-reperfusion injury (IRI). Methods: Eighteen SD rats weighing 32 0-380 g were randomly divided into three groups: ① IR group: occluded left anterior descending coronary artery for 60 min and loosening clamp for 2 min; ② ischemia / reperfusion + SMT group (SMT): 5 min before reperfusion, the iNOS inhibitor S methylisothioureasulfate (SMT 5 mg / kgw) was injected into the femoral vein, the rest were the same as the IR group; ③the control group (C): without any treatment after the heart was exposed, . The level of NO2 - + NO3- in myocardium was measured, the level of NO2 - + NO3- was measured before and after the experiment, and the myocardial tissue was examined by transmission electron microscopy. Results: The level of NO2 - + NO3 - in serum of IR group was significantly higher than that before experiment (P <0.01), NO2 - + NO3- was higher than that of C group (P <0.05). Electron microscopy, myocardial fiber over contraction, mitochondria swelling, crest fracture, disordered arrangement, vacuolar formation. The level of NO2 - + NO3 - in the SMT group was lower than that before the experiment (P <0.05), NO2 - + NO3- in the myocardium was close to the C group (P> 0.05) .0 5). Electron microscopy, myocardial ultrastructure damage was significantly improved. Mitochondria clusters, electron density increased, dense clumsy, neatly arranged, swelling and vacuolization significantly reduced. Conclusion: SMT has a protective effect on myocardial ultrastructure of IRI