Downar E, Janse M J, Durrer D
Circulation. 1977 Aug;56(2):217-24. doi: 10.1161/01.cir.56.2.217.
Subepicardial transmembrane potentials were recorded from intact pig hearts to observe the changes induced by acute ischemia. Ischemia shortened action potential duration, and decreased its amplitude, upstroke velocity, and resting potential. The cells were unresponsive after 12 to 15 minutes of coronary artery occlusion, yet near normal action potentials could be restored by flushing the occluded artery with saline as late as 40 minutes after occlusion. The unipolar extracellular electrogram reflected unresponsiveness by a monophasic potential. Local refractory periods initially shortened by up to 100 msec. Later, postrepolarization refractoriness occurred and refractory periods lengthened often in excess of basic cycle length, thus resulting in 2:1 responses. The onset of early ventricular arrhythmias often coincided with a period of alternation and 2:1 responses, especially when these got out of phase in different regions. Reperfusion frequently led to ventricular fibrillation, and was associated with marked inhomogeneity in cellular responses. Re-entry within ischemic myocardium was the most likely mechanism for arrhythmias.
从完整的猪心脏记录心外膜下跨膜电位，以观察急性缺血所引起的变化。缺血使动作电位时程缩短，并降低其幅度、除极速度和静息电位。冠状动脉闭塞12至15分钟后细胞失去反应，但在闭塞后40分钟时，用生理盐水冲洗闭塞的动脉仍可使动作电位恢复至接近正常。单极细胞外电图以单相电位反映细胞失去反应。局部不应期最初缩短达100毫秒。随后，复极后不应期出现，不应期常延长超过基本心动周期长度，从而导致2:1反应。早期室性心律失常的发作常与交替期和2:1反应同时出现，尤其是当这些现象在不同区域出现不同步时。再灌注常导致心室颤动，并与细胞反应的显著不均一性有关。缺血心肌内的折返是心律失常最可能的机制。
