Lack of change in MnSOD during ischemia/reperfusion of isolated rat heart.
Lack of change in MnSOD during ischemia/reperfusion of isolated rat heart.
复制标题
离体大鼠心脏缺血/再灌注期间 MnSOD 缺乏变化。
DOI：
10.1006/jmcc.1993.1131
复制
发表时间：
1993
影响因子：
5
通讯作者：
Ho,YS
中科院分区：
文献类型：
--
作者：
Subramanian,R;Volovsek,A;Ho,YS
内源性超氧化物歧化酶（SOD）活性降低与自由基介导的缺血心肌再灌注损伤有关。基于这一观察，抗氧化酶已被添加到急性心肌梗死再灌注治疗的方式中。采用离体大鼠心脏缺血再灌注模型，测定了不同时间缺血再灌注后MnSOD特异性蛋白含量、Mn和Cu活性、ZnSOD活性及MnSOD mRNA的表达。监测机械功能的恢复，并测定缺血前后冠状动脉流出液中乳酸和乳酸脱氢酶的释放。在可逆或不可逆的心肌损伤模型中，我们注意到心肌MnSOD特异性蛋白含量没有变化，与以前的一些观察结果相反，Mn或Cu，ZnSOD的活性水平没有变化。我们的研究结果表明，在缺血和再灌注过程中，自由基介导的心脏损伤可能不是由于受损的活动或降解的天然SOD。
Decreased endogenous superoxide dismutase (SOD) activity has been implicated in free radical-mediated reperfusion injury of the ischemic myocardium. Antioxidant enzymes have been added to the modalities of reperfusion therapy of acute myocardial infarction based on this observation. We measured the content of MnSOD specific protein, activity of Mn and Cu,ZnSODs, and MnSOD mRNA in the working isolated rat heart subjected to various durations of ischemia and reperfusion. Recovery of mechanical function was monitored and lactate and lactic dehydrogenase released in the coronary effluent before and after ischemia were measured. In this model with reversible or irreversible myocardial injury, we noted no change in the myocardial MnSOD specific protein content and, contrary to some previous observations, no change in the activity levels of Mn or Cu,ZnSODs. Our results suggest that free radical-mediated damage in the heart during ischemia and reperfusion is probably not due to impaired activity or degradation of native SODs.