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有氧运动训练可延缓糖尿病心肌梗死后大鼠的心功能障碍,并改善循环的自主神经控制。

Aerobic exercise training delays cardiac dysfunction and improves autonomic control of circulation in diabetic rats undergoing myocardial infarction.

机构信息

Human Movement Laboratory, São Judas Tadeu University, São Paulo-SP, Brazil.

出版信息

J Card Fail. 2012 Sep;18(9):734-44. doi: 10.1016/j.cardfail.2012.07.006.

Abstract

BACKGROUND

Exercise training (ET) has been used as a nonpharmacological strategy for treatment of diabetes and myocardial infarction (MI) separately. We evaluated the effects ET on functional and molecular left ventricular (LV) parameters as well as on autonomic function and mortality in diabetics after MI.

METHODS AND RESULTS

Male Wistar rats were divided into control (C), sedentary-diabetic infarcted (SDI), and trained-diabetic infarcted (TDI) groups. MI was induced after 15 days of streptozotocin-diabetes induction. Seven days after MI, the trained group underwent ET protocol (90 days, 50-70% maximal oxygen consumption-VO(2)max). LV function was evaluated noninvasively and invasively; baroreflex sensitivity, pulse interval variability, cardiac output, tissue blood flows, VEGF mRNA and protein, HIF1-α mRNA, and Ca(2+) handling proteins were measured. MI area was reduced in TDI (21 ± 4%) compared with SDI (38 ± 4%). ET induced improvement in cardiac function, hemodynamics, and tissue blood flows. These changes were probable consequences of a better expression of Ca(2+) handling proteins, increased VEGF mRNA and protein expression as well as improvement in autonomic function, that resulted in reduction of mortality in TDI (33%) compared with SDI (68%) animals.

CONCLUSIONS

ET reduced cardiac and peripheral dysfunction and preserved autonomic control in diabetic infarcted rats. Consequently, these changes resulted in improved VO(2)max and survival after MI.

摘要

背景

运动训练(ET)已被用作治疗糖尿病和心肌梗死(MI)的非药物策略。我们评估了 ET 对糖尿病 MI 后左心室(LV)功能和分子参数以及自主神经功能和死亡率的影响。

方法和结果

雄性 Wistar 大鼠分为对照组(C)、久坐型糖尿病梗死组(SDI)和训练型糖尿病梗死组(TDI)。MI 在链脲佐菌素诱导糖尿病后 15 天诱导。MI 后 7 天,训练组进行 ET 方案(90 天,50-70%最大摄氧量-VO2max)。非侵入性和侵入性评估 LV 功能;测量血压反射敏感性、脉搏间隔变异性、心输出量、组织血流、VEGF mRNA 和蛋白、HIF1-α mRNA 和 Ca2+处理蛋白。与 SDI(38±4%)相比,TDI(21±4%)的 MI 面积减少。ET 诱导心脏功能、血液动力学和组织血流改善。这些变化可能是由于 Ca2+处理蛋白表达更好、VEGF mRNA 和蛋白表达增加以及自主神经功能改善,导致 TDI(33%)的死亡率低于 SDI(68%)动物。

结论

ET 减轻了糖尿病梗死大鼠的心脏和外周功能障碍,并维持了自主神经控制。因此,这些变化导致 MI 后 VO2max 和存活率的提高。

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