MECHANISM AND TIME COURSE OF S-T AND T-Q SEGMENT CHANGES DURING ACUTE REGIONAL MYOCARDIAL ISCHEMIA IN PIG HEART DETERMINED BY EXTRACELLULAR AND INTRACELLULAR-RECORDINGS

MECHANISM AND TIME COURSE OF S-T AND T-Q SEGMENT CHANGES DURING ACUTE REGIONAL MYOCARDIAL ISCHEMIA IN PIG HEART DETERMINED BY EXTRACELLULAR AND INTRACELLULAR-RECORDINGS
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DOI:
10.1161/01.res.42.5.603
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发表时间:
1978-01-01
影响因子:
20.1
通讯作者:
DURRER, D
DURRER, D
中科院分区:
医学1区
文献类型:
--
作者:
KLEBER, AG;JANSE, MJ;DURRER, D

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在离体灌流的猪心上记录左前降支阻断前后心外膜下心室细胞的跨膜电位和局部细胞外直流电图。第一个变化是静息膜电位降低,反映为电描记图中的T-Q降低。3分钟后,动作电位缩短,幅度降低,导致S-T升高,直到最后,缺血区中心的细胞在约-65 mV的静息电位下完全无反应。这使得细胞外复合物呈单相。在150-250个心外膜部位测定闭塞15-30分钟后的细胞外电位分布,显示T-Q降低和S-T升高向中心区域增加,最大值分别为-15和+35 mV。比较壁内和心外膜电位的振幅和形态,发现在整个缺血部位的壁电位分布是均匀的。因此,细胞外心外膜电流起源于心外膜细胞内室。在收缩晚期期间的最大电流密度为1 μ A/mm 2,在边界区中流向正常心肌。闭塞1小时后,细胞外DC电位明显降低,这可能是由于缺血区电活动的短暂恢复。2小时后,无反应区大于闭塞15分钟后,DC电位的整体幅度进一步下降,可能是因为愈合。
Transmembrane potentials were recorded from subepicardial ventricular cells and local extracellular DC electrograms in isolated perfused pig hearts before and after occlusion of the left anterior descending artery. The 1st change was a decrease in the resting membrane potential, reflected by T-Q depression in the electrogram. After 3 min, action potentials shortened and their amplitude decreased, resulting in S-T elevation until, finally, cells in the center of the ischemic zone became totally unresponsive at resting potentials of about -65 mV. This rendered the extracellular complex monophasic. Determination of extracellular potential distribution at 150-250 epicardial sites after 15-30 min of occlusion showed an increase of T-Q depression and S-T elevation toward a central area, with maximum values of -15 and +35 mV, respectively. Comparison of amplitude and configuration of intramural and epicardial potential profiles revealed that the potential distribution was homogeneous throughout ischemic parts of the wall. Extracellular epicardial current originated, therefore, from the epicardial intracellular compartment. Maximal current density during late systole was 1 .mu.A/mm2, flowing in the border zone towards normal myocardium. After 1 h of occlusion, there was a marked decrease of extracellular DC potentials which could be attributed to transient recovery of electrical activity in the ischemic zone. After 2 h, the zone of unresponsiveness was larger than after 15 min of occlusion, and the overall amplitude of DC potentials had decreased further, possibly because of healing over.