有氧运动间歇训练部分逆转梗死后心力衰竭大鼠心房肌细胞的收缩功能障碍和 Ca2+处理受损。
Aerobic interval training partly reverse contractile dysfunction and impaired Ca2+ handling in atrial myocytes from rats with post infarction heart failure.
机构信息
K.G. Jebsen Center of Exercise in Medicine, Department of Circulation and Medical Imaging, Faculty of Medicine, Norwegian University of Science and Technology, Trondheim, Norway.
出版信息
PLoS One. 2013 Jun 14;8(6):e66288. doi: 10.1371/journal.pone.0066288. Print 2013.
BACKGROUND
There is limited knowledge about atrial myocyte Ca(2+) handling in the failing hearts. The aim of this study was to examine atrial myocyte contractile function and Ca(2+) handling in rats with post-infarction heart failure (HF) and to examine whether aerobic interval training could reverse a potential dysfunction.
METHODS AND RESULTS
Post-infarction HF was induced in Sprague Dawley rats by ligation of the left descending coronary artery. Atrial myocyte shortening was depressed (p<0.01) and time to relaxation was prolonged (p<0.01) in sedentary HF-rats compared to healthy controls. This was associated with decreased Ca(2+) amplitude, decreased SR Ca(2+) content, and slower Ca(2+) transient decay. Atrial myocytes from HF-rats had reduced sarcoplasmic reticulum Ca(2+) ATPase activity, increased Na(+)/Ca(2+)-exchanger activity and increased diastolic Ca(2+) leak through ryanodine receptors. High intensity aerobic interval training in HF-rats restored atrial myocyte contractile function and reversed changes in atrial Ca(2+) handling in HF.
CONCLUSION
Post infarction HF in rats causes profound impairment in atrial myocyte contractile function and Ca(2+) handling. The observed dysfunction in atrial myocytes was partly reversed after aerobic interval training.
背景
对于衰竭心脏中心房肌细胞 Ca(2+) 处理的了解有限。本研究旨在研究梗死后心力衰竭（HF）大鼠的心房肌细胞收缩功能和 Ca(2+) 处理，并研究有氧运动间歇训练是否可以逆转潜在的功能障碍。
方法和结果
通过结扎左冠状动脉降支在 Sprague Dawley 大鼠中诱导梗死后 HF。与健康对照组相比，久坐不动的 HF 大鼠的心房肌细胞缩短功能降低（p<0.01），舒张时间延长（p<0.01）。这与 Ca(2+) 幅度降低、SR Ca(2+) 含量降低以及 Ca(2+) 瞬变衰减减慢有关。HF 大鼠的心房肌细胞肌浆网 Ca(2+)ATP 酶活性降低，Na(+)/Ca(2+) 交换器活性增加，通过兰尼碱受体的舒张 Ca(2+) 渗漏增加。HF 大鼠的高强度有氧间歇训练恢复了心房肌细胞的收缩功能，并逆转了 HF 中心房 Ca(2+) 处理的变化。
结论
大鼠梗死后 HF 导致心房肌细胞收缩功能和 Ca(2+) 处理严重受损。有氧运动间歇训练后，观察到的心房肌细胞功能障碍部分得到逆转。
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