中文摘要：

目的：研究缺血后处理（postconditioning）对不同时程冷保存大鼠心脏的作用及其机制。方法：利用Langendorff离体鼠心灌注法，观察大鼠心脏在Celsior液（4C）中保存3h或5h后，在其后复灌60min期间血流动力学的恢复情况，并对复灌期间心律失常严重程度进行定量分析。缺血后处理采用全心停灌30s，复灌30s，循环3次。结果：（1）与3h冷保存对照组相比，大鼠心脏冷保存3h后给予缺血后处理，在多个复灌时间点上可明显降低左室舒张末期压力，而心率、左室发展压、左室最大收缩／舒张速率、冠脉流出量、心率与发展压的乘积等的恢复率在复灌期明显高于3h对照组。心脏冷保存3h后心律失常的发生率在复灌第0～10min时最高，缺血后处理可明显降低心律失常的发生率。（2）在缺血后处理短暂复灌期的K—H灌流液中加入100μmol／L的5-HD（线粒体ATP依赖性钾离子通道的阻断剂），可取消缺血后处理降低左室舒张末期压力，增高心率、左室发展压、左室最大收缩／舒张速率、冠脉流出量、心率与发展压乘积的作用。心律失常评分亦明显高于3h缺血后处理组。（3）大鼠心脏冷保存5h后给予缺血后处理，在复灌期间各项动力学指标以及心律失常评分上与5h冷保存对照组无明显差异。结论：缺血后处理对于3h冷保存的大鼠心脏有显著的保护作用，其作用机制可能是部分通过激活线粒体ATP依赖性钾离子通道起作用，而缺血后处理对于5h冷保存的大鼠心脏并无保护作用。

英文摘要：

Objective： To assess the effect of postconditioning on cardiac protection of rat hearts suffered from long-term hypothermic preservation. Methods： The Langendorff model of isolated rat heart was used. After 30 min of stabilization,the hearts were stored in 4 C Celsior solution for 3 or 5 h followed by 60 min of reperfusion. Postconditioning was initiated by 3 cycles of 30 s ischemia followed by 30 s reperfusion at the beginning of subsequent persistent reperfusion. The recovery of cardiac contractile function and arrhythmia score were observed. Results： （1） Compared with control group,postconditioning increased the recovery of heart rate （HR）,left ventricular systolic pressure （LVDP）,maximal rise/fall rate of ventricular pressure （dP/dtmax） and coronary flow （CF） and rate-pressure product （RPP） during reperfusion after 3 h of hypothermic preservation. However, left ventricular end-diastolic pressure （LVEDP） and the cardiac arrhythmia score during the first 10 min of reperfusion was significantly lower in 3 h postconditioning group than that in 3 h control group. （2） The rat hearts treated by postconditioning with 5-HD（100 μmol/L） abolished the amelioration of contract function induced by postconditioning. And it could also increase the cardiac arrhythmia score. （3） Compared with 5 h control group, the HR, LVDP, dP/dt CF, LVEDP, RPP and the cardiac arrhythmia score were not significantly different in postconditioning treated hearts during reperfusion after 5 h of hypothermic preservation. Conclusion： Postconditioning could provide the cardiac protection on 3 h hypothermic preserved rat hearts,but not on 5 h hypothermic preserved rat hearts. The cardiac protection effect might be partly associated with activation of selective mitochondrial ATP -sensitive potassium channel.