Elevated MnSOD is not required for exercise-induced cardioprotection against myocardial stunning.

Elevated MnSOD is not required for exercise-induced cardioprotection against myocardial stunning.
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运动引起的心脏保护作用不需要升高 MnSOD 来防止心肌顿抑。

DOI:
10.1152/ajpheart.01208.2003
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发表时间:
2004
期刊:
American journal of physiology. Heart and circulatory physiology
影响因子:
--
通讯作者:
Powers,ScottK
Powers,ScottK
中科院分区:
--
文献类型:
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作者:
Lennon,ShannonL;Quindry,JohnC;Hamilton,KarynL;French,JoelP;Hughes,Jeffrey;Mehta,JayL;Powers,ScottK

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耐力运动对缺血再灌注引起的心肌顿抑和梗死具有心脏保护作用。最近的一项研究表明,运动引起的心肌锰超氧化物歧化酶(MnSOD)活性的增加是必不可少的,以保护心脏免受梗死。目前尚不清楚心脏MnSOD的升高是否也是实现运动诱导的心肌顿抑保护的先决条件。因此,本研究确定了运动诱导的心肌MnSOD活性增加是否是实现心肌顿抑保护的必要条件。成年雄性大鼠保持久坐不动或进行连续的耐力运动。将心脏暴露于25分钟的全脑缺血,然后在分离的工作心脏制备中再灌注。与静坐对照组相比,运动动物在再灌注期间的缺血后心脏外功恢复显著更高(84 ± 3 vs. 67 ± 4%)。此外,通过反义寡核苷酸阻止运动诱导的心肌MnSOD表达并没有阻碍这种运动诱导的心肌顿抑保护作用。这些数据表明,运动引起的心脏MnSOD活性的增加是不必要的,以实现运动介导的保护心肌顿抑。因此,我们得出结论,不同的介质负责运动诱导的心肌保护对心肌顿抑和梗死。
Endurance exercise provides cardioprotection against ischemia-reperfusion-induced myocardial stunning and infarction. A recent study demonstrates that an exercise-induced increase in myocardial manganese superoxide dismutase (MnSOD) activity is essential to protect the heart against infarction. It is unknown if an elevation in cardiac MnSOD is also a prerequisite to achieve exercise-induced protection against myocardial stunning. Therefore, this study determined if an exercise-induced increase in myocardial MnSOD activity is a requirement to achieve protection against myocardial stunning. Adult male rats remained sedentary or performed successive bouts of endurance exercise. Hearts were exposed to 25 min of global ischemia followed by reperfusion in an isolated working heart preparation. Postischemic recovery of cardiac external work during reperfusion was significantly higher (84 ± 3 vs. 67 ± 4%) in exercised animals compared with sedentary controls. Furthermore, prevention of exercise-induced expression of myocardial MnSOD via antisense oligonucleotides did not retard this exercise-induced protection against myocardial stunning. These data demonstrate that exercise-induced increases in cardiac MnSOD activity are not essential to achieve exercise-mediated protection against myocardial stunning. Therefore, we conclude that different mediators are responsible for exercise-induced cardioprotection against myocardial stunning and infarction.