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目的 探讨Na+ H+ 交换抑制剂二甲基阿米洛利 (DMA)对心肌缺血 再灌注损伤(MIRI)的影响。方法 离体鼠心脏置于Langendorff装置上 ,采用主动脉逆灌法 ,停灌 30min后复灌30min ,造成MIRI模型。离体鼠心脏稳定灌流 2 0min ,随机分成 4组 :对照组、DMA 5 μmol L组、10 μmol L组和 2 0 μmol L组 ,每组各 8例。记录心电图和心肌收缩力的变化 ,测定缺血前及再灌注30min时冠脉流出量以及心肌组织含钙量 ,观察心肌细胞超微结构变化。结果 与对照组相比 ,DMA10 μmol L组和 2 0 μmol L组心率、心肌收缩力和冠脉流出量的恢复程度明显提高 (P <0 0 5或0 0 1) ,心律失常发生率及心肌组织钙含量明显降低 (P <0 0 5或 0 0 1) ,超微结构改变轻微 ,而DMA5 μmol L组仅在再灌注 10min和 15min时心肌收缩力恢复程度高于对照组 (P <0 0 5 ) ,其他指标均无显著性变化。结论 DMA对心肌缺血 再灌注损伤有一定的保护作用 ,且与剂量有关
Objective To investigate the effect of Na + H + exchange inhibitor dimethyl amiloride (DMA) on myocardial ischemia-reperfusion injury (MIRI). Methods The isolated rat heart was placed on a Langendorff apparatus. The aortic instillation method was used. After 30 min of reperfusion, reperfusion was performed for 30 min, resulting in MIRI model. The hearts of isolated mice were perfused for 20 min and were randomly divided into 4 groups: control group, DMA 5 μmol L group, 10 μmol L group and 20 μmol L group, 8 cases in each group. The changes of electrocardiogram and myocardial contractility were recorded. The coronary outflow and the content of calcium in myocardium before ischemia and 30 minutes after reperfusion were measured. The ultrastructural changes of myocardial cells were observed. Results Compared with the control group, the recovery of heart rate, myocardial contractility and coronary outflow increased significantly in DMA10 μmol L group and 20 μmol L group (P <0.05 or 0.01), arrhythmia incidence and myocardial (P <0 05 or 0 0 1), and slight changes in ultrastructure. Compared with the control group, myocardial contractility of DMA5 μmol L group was only restored at 10 min and 15 min after reperfusion 5), no significant change in other indicators. Conclusion DMA has a protective effect on myocardial ischemia-reperfusion injury, and dose-related