预处理对心肌细胞的保护作用

Effects of Hypoxic or Ischemic Preconditioning on Cardiomyocytes

为探讨缺氧和缺血预处理对心肌细胞的保护作用 ,分别在培养的乳鼠心肌细胞缺氧 复氧模型、离体大鼠灌注和在体大鼠心肌缺血 再灌注模型中 ,观察缺血和缺氧预处理对心肌细胞再次长时间缺氧 复氧或缺血 再灌注损伤的保护作用。结果发现 ,在培养的乳鼠心肌细胞中 ,缺氧预处理组细胞存活率和超氧化物歧化酶含量较缺氧 复氧组增加 (P <0 .0 1) ,乳酸脱氢酶的释放和丙二醛含量则减少 (P <0 .0 1)。对离体或在体大鼠心脏的缺血预处理也可减少长时间缺血 再灌注对心肌细胞的损伤。离体大鼠缺血预处理组冠状动脉流出液中乳酸脱氢酶的释放和组织丙二醛的含量较非预处理组减少 (P <0 .0 1) ,心脏的湿干重比和组织超氧化物歧化酶含量则增加 (P <0 .0 1)。在体大鼠心肌缺血预处理组梗死范围和血清乳酸脱氢酶较缺血 再灌注组减少 (P <0 .0 1) ,无论是再次缺血还是再灌注期室性心律失常的发生率在预处理组明显低于非预处理组 (P <0 .0 1)。结果提示 ,缺血或缺氧预处理对心肌具有保护作用 ,预处理可以减少再次长时间的缺氧 复氧或缺血

Aim To investigate the effects of hypoxic or ischemic preconditioning on cardiomyocytes. Methods In the hypoxia/reoxygenation (H/R) model of cultured neonatal rat cardi omyocytes, and the ischemia/reperfusion (I/S) model of the isolated or in situ rat hearts, the present study observes the effects of PC on H/R or I/R injury on cardiomyocytes. The infarct size, cell viability, LDH release and the content of MDA were measured. Results Hypoxia PC attenuated H/R injuries on cardiomyocytes. On the model of cultured neonatal rat cardiomyocytes, compared with the cardiomyocytes unpreconditioned, the number of viable cell and the SOD content were increased (P<0.01), the LDH release and the MDA content were decreased (P<0.01) in preconditioned group. In isolated or in situ rat hearts, ischemic PC decreased the injuries to cardiomyocytes. The coronary artery effusion or plasma LDH levels, tissue MDA contents, the infarct sizes and arrhythmia during occlusion or reperfusion were greatly decreased in preconditioned myocardium after a long time I/R than those in the unpreconditioned (P< 0.01). Conclusions Cultured neonatal rat cardiomyocytes, isolated and in situ rat hearts have PC phenomenon. PC can obviously protect cultured neonatal rat cardiomyocytes, isolated or in situ rat heart from H/R or I/R injuries.