EXCITATION-CONTRACTION COUPLING IN POSTISCHEMIC MYOCARDIUM - DOES FAILURE OF ACTIVATOR CA-2+ TRANSIENTS UNDERLIE STUNNING
EXCITATION-CONTRACTION COUPLING IN POSTISCHEMIC MYOCARDIUM - DOES FAILURE OF ACTIVATOR CA-2+ TRANSIENTS UNDERLIE STUNNING
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DOI：
10.1161/01.res.66.5.1268
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发表时间：
1990-05-01
影响因子：
20.1
通讯作者：
MARBAN, E
中科院分区：
文献类型：
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作者：
KUSUOKA, H;KORETSUNE, Y;MARBAN, E
为了阐明缺血后心肌收缩功能障碍的机制，使用门控19 F核磁共振在7个灌注的雪貂心脏中进行了细胞内游离Ca 2+浓度（[Ca 2 +]i）的时间分辨测量，其中灌注的雪貂心脏装载有氟化Ca 2+指示剂5 F-BAPTA。左心室发展压降至65 ± 0.05。3%（平均值±）。对照组在37 ℃下全脑缺血15分钟后的扫描电镜（SEM）。C.顿抑心肌舒张期[Ca ~（2+）]i为0.24 ± 0.25; 0.03相对于对照组（0.18 ± 0.18 μ M）没有变化。0.03μ M，p > 0.10），但峰值[Ca 2 +]i（1.03 ± 0.01）。0.13相反地，在对照中（0.61 ± 0.001 μ M）高于对照（0.61 ± 0.001 μ M）。0.06μ M，p < 0.02）。顿抑心肌的动态压力与Ca ~（2+）瞬时振幅的关系斜率显著低于对照组（P < 0.05），即使在最大Ca ~（2+）激活压力恢复正常后也是如此。这些结果表明，在顿抑心肌收缩失败是由于压力的肌丝对Ca 2+的敏感性，以及先前确定的最大Ca 2+激活力的减少;激活剂Ca 2+的交付失败不能牵连。Ca 2+瞬变幅度的增加将需要更多的ATP用于Ca 2+螯合;因此，将导致顿抑心肌的能量利用效率降低。
To elucidate the mechanism of contractile dysfunction in postischemic ("stunned") myocardium, time-resolved measurements of intracellular free Ca2+ concentration ([Ca2+]i) were made using gated 19F nuclear magnetic resonance in seven perfused ferret hearts loaded with the fluorinated Ca2+ indicator 5F-BAPTA. Left ventricular developed pressure decreased to 65 .+-. 3% (mean .+-. SEM) of control after 15 minutes of global ischemia at 37.degree. C. In stunned myocardium, diastolic [Ca2+]i (0.24 .+-. 0.03 .mu.M) was not changed from control (0.18 .+-. 0.03 .mu.M, p > 0.10), but peak [Ca2+]i (1.03 .+-. 0.13 .mu.M) was paradoxically higher than that in control (0.61 .+-. 0.06 .mu.M, p < 0.02). The slope of the relation between developed pressure and Ca2+ transient amplitude in stunned myocardium was significantly lower than that in control (p < 0.05), even after normalization by maximal Ca2+-activated pressure. These results indicate that contractile failure in stunned myocardium is due to a pressure in the myofilament sensitivity to Ca2+ as well as to the previously identified decrease in maximal Ca2+-activated force; failure of activator Ca2+ delivery cannot be implicated. The increase in the amplitude of Ca2+ transients would require that more ATP be spent in Ca2+ sequestration; thus, decreased efficiency of energy utilization in stunned myocardium would result.