Prolonged mechanical unloading affects cardiomyocyte excitation-contraction coupling, transverse-tubule structure, and the cell surface
Prolonged mechanical unloading affects cardiomyocyte excitation-contraction coupling, transverse-tubule structure, and the cell surface
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DOI：
10.1096/fj.10-156638
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发表时间：
2010-09-01
期刊：
影响因子：
4.8
通讯作者：
Terracciano, Cesare M. N.
中科院分区：
文献类型：
--
作者：
Ibrahim, Michael;Al Masri, Abeer;Terracciano, Cesare M. N.
心脏的长时间机械卸载（UN）与心肌细胞结构和功能的有害变化有关。这些变化背后的机制尚不清楚。在这项研究中，我们报告了UN对兴奋-收缩偶联，特别是Ca 2+诱导的Ca 2+释放（CICR）和横（t）-小管结构的影响。采用雄性刘易斯大鼠腹腔异位心脏移植术诱导UN。4周后从移植心脏中分离左心室心肌细胞，并使用全细胞膜片钳、共聚焦显微镜和扫描离子电导显微镜（SICM）进行研究。心脏移植作为对照（C）。UN组心肌细胞体积较C组减少56.5%（UN，n = 90; C，n = 59; P
Prolonged mechanical unloading (UN) of the heart is associated with detrimental changes to the structure and function of cardiomyocytes. The mechanisms underlying these changes are unknown. In this study, we report the influence of UN on excitation-contraction coupling, Ca2+-induce Ca2+ release (CICR) in particular, and transverse (t)-tubule structure. UN was induced in male Lewis rat hearts by heterotopic abdominal heart transplantation. Left ventricular cardiomyocytes were isolated from the transplanted hearts after 4 wk and studied using whole-cell patch clamping, confocal microscopy, and scanning ion conductance microscopy (SICM). Recipient hearts were used as control (C). UN reduced the volume of cardiomyocytes by 56.5% compared with C (UN, n = 90; C, n = 59; P