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目的:对比研究心肌肌膜和线粒体ATP敏感性钾通道(KA+TP)在缺血预适应(IP)对小鼠体外心脏缺血/再灌注(I/R)损伤后梗死范围、心律失常和心功能的影响。方法:采用改良的Langendorff小鼠心脏灌注系统同步记录C57BL/6小鼠心脏心电图、左心室发展压和左心室压发展速率。选用特异性心肌肌膜KA+TP阻断剂HMR109830μmol/L和特异性心肌线粒体KA+TP阻断剂5HD500μmol/L。分对照组、IP组、IP加HMR1098组和IP加5HD组。IP组稳定16min后,行2个循环的IP,缺血2min和再灌注5min;然后缺血20min和再灌注45min,对照组无IP。在45min再灌注结束后,测定心肌梗死范围。结果:与对照组相比,IP组能显著降低心肌梗死范围,分别为(38·1±1·82)%和(29·4±2·71)%(P<0·05),但对心律失常积分和心功能恢复无明显影响。与IP组相比,IP加HMR1098组和IP加5HD组能显著增加心肌梗死范围和降低心功能,心肌梗死范围分别为(45·6±4·7)%和(51·1±5·2)%,但2组间差异无统计学意义。结论:IP对小鼠体外心脏I/R损伤具有保护作用,心肌肌膜和线粒体KA+TP在IP后I/R损伤过程中均起重要作用。心肌梗死范围可作为IP保护心肌的可靠指标,但要慎重对待心律失常和心功能的变化。
OBJECTIVE: To compare the effects of ischemic preconditioning (IP) on myocardium and mitochondrial ATP-sensitive potassium channels (KA + TP) on infarct size, arrhythmia and myocardial infarction in mice after myocardial ischemia / reperfusion (I / R) Impact of heart function. Methods: Cardiac electrocardiogram, left ventricular development pressure and left ventricular pressure were recorded synchronously in C57BL / 6 mice with a modified Langendorff mouse heart perfusion system. Selection of specific myocardial sarcolemma KA + TP blockers HMR109830μmol / L and specific myocardial mitochondrial KA + TP blockers 5HD500μmol / L. The control group, IP group, IP plus HMR1098 group and IP plus 5HD group. IP group stable 16min, the line 2 IP, ischemia 2min and reperfusion 5min; then ischemia 20min and reperfusion 45min, the control group without IP. After 45 min of reperfusion, the infarct size was determined. Results: Compared with the control group, IP group could significantly reduce the range of myocardial infarction (38.1 ± 1.82%) and (29.4 ± 2.71)% (P <0.05) Arrhythmia scores and heart function recovery had no significant effect. Compared with IP group, IP plus HMR1098 group and IP plus 5HD group could significantly increase the range of myocardial infarction and reduce the cardiac function, the ranges of myocardial infarction were (45.6 ± 4.77)% and (51.1 ± 5.2) )%, But no significant difference between the two groups. CONCLUSION: IP has a protective effect on I / R injury in vitro. Myocardium and mitochondrial KA + TP play an important role in I / R injury after IP. Myocardial infarction range can be used as a reliable indicator of IP protection of myocardium, but careful treatment of arrhythmias and changes in cardiac function.