超氧化物歧化酶在心肌再灌注性损伤中的作用

Reduction of myocardial postisehemic reperfusion injury with superoxide dismutase

本实验在大鼠离体心脏灌注模型上,模拟心肌缺血再灌注过程(旷置30分钟,再灌注45分钟),结果发现:再灌注后,心脏频发室颤,组织水肿明显,脂质过氧化终产物丙二醛较正常时显著增加,冠脉流出液中乳酸脱氢酶呈一持续高水平释放,心肌组织ATP酶活性明显下降。再灌注开始后给予超氧化物歧化酶(SOD)。能够减轻以上心肌再灌注性损伤现象。这一结果提示:1)活性氧参与了心肌再灌注损伤现象的发生。2)再灌注开始后给予SOD仍有明显疗效,这为临床上在再灌注开始后应用SOD提供了一定的实验依据。

Activated oxygen has been proposed to play a role in postischemic cardiac damage. This is supported further by the ability of activated oxygen scavengers to limit myocardial reperfusion injury. This experiment was performed to determine if superoxide dismutase (SOD) infused starting with reperfusion has a beneficial effect on reperfused myocardiun?The isolated perfused rat hearts were subjected to ischemia followed by reperfusion for 45 min. Reperfusion damage was detected by occurrence of ventricular fibrillation, increase production of malondialdehyde, the release of lactate dehydrogenase and the reduction of sarcolemmal ATPase. The extent of reperfusion myocardial injury was significantly less in SOD treated group indicated by the indics mentioned above. The results of this study are in accord with previous concepts that activated oxygen plays a fundamental role in cellular damage resulted from reperfusion. In addition, we demonstrate that the administration of SOD begining at the onset of reperfusion can still be effective, it might be applicable to clinical case.