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首页> 外文期刊>American Journal of Physiology >Elevated MnSOD is not required for exercise-induced cardioprotection against myocardial stunning.
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Elevated MnSOD is not required for exercise-induced cardioprotection against myocardial stunning.

机译：运动诱导的抗心肌电击的心肌保护不需要高浓度的MnSOD。

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摘要

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.
机译：耐力运动可保护心肌免受缺血再灌注引起的心肌电击和梗塞。最近的研究表明，运动引起的心肌锰超氧化物歧化酶（MnSOD）活性的增加对于保护心脏免于梗塞至关重要。尚不清楚心脏MnSOD的升高是否也是获得运动诱导的抗心肌电击保护的先决条件。因此，这项研究确定了运动诱导的心肌MnSOD活性的增加是否是实现保护心肌免于击晕的必要条件。成年雄性大鼠久坐不动或连续进行耐力运动。使心脏暴露于25分钟的整体缺血，然后在孤立的工作心脏制剂中进行再灌注。与久坐的对照组相比，运动动物的缺血再灌注期间心脏外部工作的恢复显着更高（84 +/- 3比67 +/- 4％）。此外，通过反义寡核苷酸防止运动诱导的心肌MnSOD表达并不妨碍这种运动诱导的针对心肌电击的保护作用。这些数据表明，运动引起的心脏MnSOD活性增加对于实现运动介导的抗心肌电击保护不是必需的。因此，我们得出的结论是，不同的介体负责运动诱发的针对心肌电晕和梗塞的心脏保护作用。

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