【摘要】 目的探讨多聚ADP腺苷合成酶(poly ADP-ribose synthetase,PARS)抑制剂PJ34联合镁钾心停搏液对老年心肌的保护作用。方法建立老年兔Lngendorff离体灌注模型,分4组进行实验:A组为全心缺血-再灌注组,B组为镁钾心停搏液诱导停跳组,C组为PJ34保护组,D组为PJ34联合镁钾心停搏液保护组。比较各组左心室舒展末期压(left ventricular end-diastolic pressure,LVEDP)、左心室峰发展压(left ventricular peak-de-veloped pressure,LVPDP)、左室压力上升速率(the positive first derivative of pressure over time,+dp/dt)、冠脉流量(coronary flow,CF)、心肌梗死量(infarction volume,IV)、心肌组织湿重/干重比。结果左心功能恢复以D组最佳,明显优于其他组(P<0.05)。四组IV分别为:(32.8±1.6)%(A组)、(25.2±1.3)%(B组)、(13.4±0.7)%(C组)、(12.3±0.5)%(D组),以D组最少,明显少于其他三组(P<0.05)。结论PARS抑制剂PJ34联合镁钾心停搏液,能改善左心功能恢复,降低IV,减轻心肌损伤,有可能为另一种有效的心肌保护方法。更多还原

【Abstract】 Objective To investigate the protection of rabbit aging myocardium by PARS inhibitor(PJ34)combined with K/Mg cardioplegia. Methods Rabbit heart was used for langendorff perfusion. Hearts were subjected to ischemia for 30 minutes followed by reperfusion for 90 minutes in group 1, or were arrested with K/Mg cardioplegia before ischemia in group 2, or perfused with PJ34 before ischemia in group 3, or perfused with PJ34 plus K/Mg cardioplegia before ischemia in group 4. Results Left ventricular function recovery was significantly improved in group 4 compared to other groups (P<0.05). Infarct size was also significantly reduced in group 4 as compared with other groups (P<0.05).Conclusion PARS inhibitor (PJ34)combined with K/Mg cardioplegia renders the heart more tolerant to ischemia-reperfusion injury. This combination might be an alternative effective myocardial protection strategy.更多还原