DEVELOPMENT OF AN ENDOCARDIAL-EPICARDIAL GRADIENT OF ACTIVATION RATE DURING ELECTRICALLY INDUCED, SUSTAINED VENTRICULAR-FIBRILLATION IN DOGS
DEVELOPMENT OF AN ENDOCARDIAL-EPICARDIAL GRADIENT OF ACTIVATION RATE DURING ELECTRICALLY INDUCED, SUSTAINED VENTRICULAR-FIBRILLATION IN DOGS
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DOI：
10.1016/0002-9149(85)90162-6
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发表时间：
1985-01-01
影响因子：
2.8
通讯作者：
IDEKER, RE
中科院分区：
文献类型：
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作者：
WORLEY, SJ;SWAIN, JL;IDEKER, RE
目前可用的电极记录的电描记图在心室颤动（VF）发作后不久变得模糊不清;因此，对VF期间的跨壁心肌去极化知之甚少。开发了一种插入电极系统（插入），用于记录VF期间的离散偏转。在20只开胸犬中，使用单次过早电击诱导VF后，使用这些骤降记录20分钟。前6只狗的心外膜暴露于室温，14只狗的透壁温度保持在38 ℃。C.在所有犬的早期VF中，记录的透壁性搏动的电描记图均包含尖锐、离散的偏转。在接下来的20分钟的VF中，电描记图中的频率、周期长度的规律性和偏转的离散性随着时间的推移而降低，首先在心外膜水平，然后向心内膜更深。在所有犬中，在整个记录期间，大多数内膜下电图中持续存在离散、规则、快速偏转。在8只犬中，在纤颤前和纤颤发作后间隔时间进行透壁心肌活检样品。在VF期间，心肌的高能磷酸盐含量降低，心外膜和心内膜半部分的降低程度相当。通过心肺转流术在另外6只犬的VF的前20分钟内维持冠状动脉灌注。在旁路上没有形成激活率的梯度，但在停止旁路的1分钟内确实形成了激活率的梯度。VF期间的心内膜-心外膜激动率梯度是由缺血引起的。它不是由缺血中的透壁差异引起的，如VF期间高能磷酸盐化合物的均匀透壁减少所证明的，也不是由透壁温度差异引起的。内分泌在VF的维持中起主导作用。
Electrograms recorded with currently available electrodes become indistinct soon after the onset of ventricular fibrillation (VF); thus, little is known about transmural myocardial depolarization during VF. A plunge electrode system (plunge) was developed that registers discrete deflections during VF. These plunges were used to record for 20 min. after inducing VF with a single premature shock in 20 open-chest dogs. In the first 6 dogs the epicardium was exposed to room temperature and in 14 dogs transmural temperature was maintained at 38.degree. C. Electrograms recorded with the transmural plunges contained sharp, discrete deflections during early VF in all dogs. Over the next 20 min. of VF, the rate, regularity of cycle length and discreteness of the deflections in the electrograms decreased with time, first at the epicardial level, then deeper toward the endocardium. In all dogs, discrete, regular, rapid-deflections persisted in the most subendocardial electrogram thoughout the recording period. In 8 dogs, transmural myocardial biopsy samples were taken before fibrillation, and at intervals after the onset of fibrillation. The high-energy phosphate content of the myocardium decreased during VF, with comparable decreases in the epicardial and endocardial halves. Coronary perfusion was maintained during the first 20 min. of VF in 6 additional dogs by cardiopulmonary bypass. A gradient of activation rates did not develop on bypass, but did develop within 1 minute of halting bypass. The endocardial-epicardial gradient of activation rates during VF is caused by ischemia. It is not caused by transmural differences in ischemia, as evidenced by the homogeneous transmural decrease in high-energy phosphate compounds during VF, nor is it caused by transmural differences in temperature. The endocardium plays a dominant role in the maintenance of VF.