Alterations of excitation-contraction coupling in stunned myocardium and in failing myocardium.
Alterations of excitation-contraction coupling in stunned myocardium and in failing myocardium.
复制标题
顿挫心肌和衰竭心肌中兴奋-收缩耦合的改变。
DOI：
10.1016/0022-2828(95)90085-3
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发表时间：
1995
影响因子：
5
通讯作者：
Marban,E
中科院分区：
文献类型：
--
作者：
Atar,D;Gao,WD;Marban,E
D.阿塔尔湾D. Gao和E.马尔班顿抑和衰竭心肌兴奋-收缩偶联的变化分子和细胞心脏病学杂志（1995）27，783-791。虽然心肌顿抑和慢性心力衰竭的特点是收缩功能障碍，有深刻的差异，其潜在的机制。心脏收缩力的变化可以通过调节细胞内[Ca 2 +]或通过改变收缩蛋白对细胞内Ca 2+的反应来实现。新的证据表明，顿抑心肌的主要损伤位于收缩蛋白水平，这可能是由蛋白酶在再灌注早期激活损伤。相反，已知衰竭心肌显示异常的细胞内Ca 2+处理，指示肌浆网功能障碍。基因表达的改变和肌丝的同种型转换也发生在心肌衰竭，与观察到的过桥循环动力学的转变一致。总之，细胞内Ca 2+稳态和肌丝功能的变化发生在失败的心肌，而顿抑心肌主要反映了Ca 2+和收缩力之间的解偶联。
D. Atar, W. D. Gao and E. Marban. Alterations of Excitation—Contraction Coupling in Stunned Myocardium and in Failing Myocardium. Journal of Molecular and Cellular Cardiology (1995) 27, 783–791. Although both myocardial stunning and chronic heart failure are characterized by contractile dysfunction, there are profound differences in their underlying mechanisms. Changes in cardiac contractile force can be effected by modulation of intracellular [Ca2+] or by alteration of the contractile protein response to intracellular Ca2+. New evidence suggests that the principal lesion in the stunned myocardium resides at the level of the contractile proteins, which may be injured by proteases activated early during reperfusion. In contrast, failing myocardium is known to display abnormal intracellular Ca2+handling, indicative of dysfunction of the sarcoplasmic reticulum. Alterations of gene expression and isoform switching of the myofilaments also occur in failing myocardium, consistent with an observed shift of the kinetics of crossbridge cycling. In conclusion, changes in both intracellular Ca2+homeostasis and myofilament function occur in failing myocardium, while stunned myocardium primarily reflects an uncoupling between Ca2+and contractile force.
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影响因子：
9.5
作者：
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DOI：
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发表时间：
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期刊：
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影响因子：
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作者：
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影响因子：
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作者：
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