Spatial heterogeneity of action potential alternans during global ischemia in the rabbit heart.
Spatial heterogeneity of action potential alternans during global ischemia in the rabbit heart.
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DOI：
10.1152/ajpheart.00369.2003
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发表时间：
2003-12
期刊：
影响因子：
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通讯作者：
Y. Qian;R. Sung;Shien‐Fong Lin;R. Province;W. Clusin
中科院分区：
文献类型：
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作者：
Y. Qian;R. Sung;Shien‐Fong Lin;R. Province;W. Clusin
心肌缺血引起动作电位时程（APD）电交替的搏动波动，从而导致T波电交替和心律失常。在两个部位发生的APD交替是特别重要的，但大多数APD交替研究涉及正常心肌的快速起搏，而不是缺血。为了确定缺血期间APD交替的空间特征，用4-[β-[2（二正丁基氨基）-6-萘基]乙烯基]吡啶鎓（di-4-ANEPPS）对血液灌注的兔心脏进行染色，并用高分辨率相机成像。在37 ℃下用充氧的台氏液灌注心脏进行染色，然后转换为50：50%血液/台氏液混合物。以3/s的速度从右心室起搏心脏，并通过停止血流6分钟使其缺血。以300帧/s的速度获得10，000像素的图像。通过固定和手动选择未失真的单像素记录来控制运动伪影。通过计算机图像处理显示上行传播和传导等时线。7个心脏中有6个显示APD交替，3个心脏在图像的不同区域呈异相。去极化至50%复极化起始（APD 50）的最大空间变异为155%。这引起了复极化的逐搏逆转。可以为图像的固定良好的部分构建交替映射。APD交替的离散区域由边界分开，如细胞内Ca 2+浓度交替。像素接近1.1 mm显示APD交替，是异相的。反相APD交替不是由于传导交替，如向上行程间期和传导等时线所示。这与快速起搏形成对比，后者似乎存在因果关系。这些新的观察结果表明，缺血期间心律失常的发生不同的机制。
Cardiac ischemia causes beat-to-beat fluctuation in action potential duration (APD) alternans, which leads to T wave alternans and arrhythmias. Occurrence of APD alternans that is out of phase at two sites is especially important, but most APD alternans studies have involved rapid pacing of normal myocardium rather than ischemia. To determine the spatial features of APD alternans during ischemia, blood-perfused rabbit hearts were stained with 4-[beta-[2(di-n-butylamino)-6-napthyl]vinyl]pyridinium (di-4-ANEPPS) and imaged with a high-resolution camera. Hearts were perfused with oxygenated Tyrode solution at 37 degrees C for staining and then switched to a 50:50% blood/Tyrode mixture. Hearts were paced from the right ventricle at 3/s, and made ischemic by stopping flow for 6 min. Images of 10,000 pixels were obtained at 300 frames/s. Motion artifact was controlled by immobilization and by manual selection of undistorted single-pixel records. Upstroke propagation and conduction isochrones were displayed by computerized image processing. APD alternans was demonstrated in six of seven hearts, and was out of phase in different regions of the image in three hearts. The largest spatial variation in the onset of depolarization to 50% repolarization (APD50) was 155%. This caused beat-to-beat reversal of repolarization. An alternans map could be constructed for well-immobilized portions of the image. There were discrete regions of APD alternans separated by a boundary, as occurs with intracellular Ca2+ concentration alternans. Pixels as close together as 1.1 mm showed an APD alternans that was out of phase. The out-of-phase APD alternans was not due to conduction alternans, as shown by upstroke intervals and conduction isochrones. This contrasts with rapid pacing, where a causal relationship appears to exist. These new observations suggest distinct mechanisms for the genesis of arrhythmias during ischemia.