Simultaneous recording of action potentials from endocardium and epicardium during ischemia in the isolated cat ventricle: relation of temporal electrophysiologic heterogeneities to arrhythmias.
Simultaneous recording of action potentials from endocardium and epicardium during ischemia in the isolated cat ventricle: relation of temporal electrophysiologic heterogeneities to arrhythmias.
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在离体猫心室缺血期间同时记录心内膜和心外膜的动作电位：时间电生理异质性与心律失常的关系。
DOI：
10.1161/01.cir.74.2.401
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发表时间：
1986
期刊：
影响因子：
37.8
通讯作者：
Myerburg,RJ
中科院分区：
文献类型：
--
作者：
Kimura,S;Bassett,AL;Kohya,T;Kozlovskis,PL;Myerburg,RJ
我们研究了缺血对冠状动脉灌注猫左心室心内膜和心外膜肌细胞跨膜动作电位、传导时间和不应期的影响。通过左冠状动脉前降支灌注含氧的 Tyrode 溶液，同时用充有 95% N2 和 5% CO2 的 Tyrode 溶液灌注制剂。在冠状动脉灌注期间，从心内膜和心外膜细胞同时记录的跨膜动作电位是正常的。当灌注停止（“缺血”）时，在心内膜和心外膜细胞中观察到动作电位快速恶化和传导时间延长。尽管静息膜电位的变化几乎相同，但心外膜细胞的动作电位幅度和动作电位持续时间（APD）的降低幅度以及传导时间的延长幅度大于心内膜细胞。然而，心内膜细胞的APD在缺血30分钟内逐渐降低，而心外膜细胞的APD在10分钟时降低最大，然后部分恢复。心内膜细胞不应期的缩短与APD的缩短是平行的，而心外膜细胞的不应期在前10分钟内减少，然后增加。缺血10 min时，心外膜细胞的APD和不应期明显短于心内膜细胞。缺血 30 分钟时，心外膜细胞的不应期超过了心内膜细胞，因为心外膜细胞出现了更大的复极不应期。伴随着心内膜和心外膜细胞的 APD 和不应期的这些不同变化，自发性期外收缩冲动增加，并且额外刺激可以诱发收缩期外冲动的快速运行。（摘要截断为 250 字）
We studied the effects of ischemia on transmembrane action potentials, conduction time, and refractory periods of both endocardial and epicardial muscle cells of coronary-perfused cat left ventricles. Oxygenated Tyrode's solution was perfused through the left anterior descending coronary artery, while the preparation was superfused with Tyrode's solution gassed with 95% N2 and 5% CO2. Transmembrane action potentials recorded simultaneously from endocardial and epicardial cells were normal during coronary perfusion. When perfusion was discontinued ("ischemia"), rapid deterioration of action potentials and prolongation of conduction time were observed in both endocardial and epicardial cells. The magnitude of the reduction of action potential amplitude and action potential duration (APD), and of prolongation of conduction time, was greater in epicardial cells than in endocardial cells, although the change in resting membrane potential was almost the same. However, APD of endocardial cells decreased progressively during 30 min of ischemia, whereas APD of epicardial cells was reduced maximally at 10 min and then partially recovered. Shortening of refractory periods of endocardial cells paralleled APD shortening, whereas refractory periods of epicardial cells decreased for the first 10 min and then increased. At 10 min of ischemia, APD and refractory periods of epicardial cells were significantly shorter than those of endocardial cells. At 30 min of ischemia, refractory periods of epicardial cells exceeded those of endocardial cells because of development of greater postrepolarization refractoriness in epicardial cells. Accompanying these different changes in APD and refractory periods of endocardial and epicardial cells, spontaneous extrasystolic impulses increased and rapid runs of extrasystolic impulses could be induced by extrastimuli.(ABSTRACT TRUNCATED AT 250 WORDS)
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