Electrophysiological alternans and restitution during acute regional ischaemia in myocardium of anaesthetized pig.
Electrophysiological alternans and restitution during acute regional ischaemia in myocardium of anaesthetized pig.
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麻醉猪心肌急性局部缺血期间的电生理交替和恢复。
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发表时间：
1988
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通讯作者：
M. Lab
中科院分区：
文献类型：
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作者：
S. Dilly;M. Lab
1.交替的长和短动作电位持续时间，或电交替，只是偶尔在原位缺血心肌观察。我们系统地研究了交替在后者的特点的现象，将其与室性心律失常，并提出可能的机制。2.将16头长白猪麻醉（Azaperone、N2 O和O2），通气并暴露心脏。结扎左冠状动脉的一个分支。监测左心室和体循环压力。单相动作电位同时记录多达五个吸力电极在和周围的拟议缺血区。3.在缺血的第一个小时内，计算机在复极的几个阶段测量每个动作电位的持续时间。这使得对交替的系统研究成为可能。在定义的刺激协议期间的测量也被用于构建电恢复曲线。4.在缺血区域内的所有记录中以及在“边界”区域的三分之二中发现了交替糖。非缺血区域无交替。5.交替，当动作电位时程绘制为每一拍，出现作为一个振荡，这是多形性。它可以是：（a）稳定数百次搏动;（B）在具有高交替和具有低交替或无交替的一个稳定状态之间切换或触发（通过具有不同周期长度的一个外来搏动）;（c）阻尼;（d）非阻尼以采取渐强形式，有时在心室颤动之前。6.交替发作通常在缺血发作后约200 - 1500次搏动之间出现不明确的峰值，在约3000次搏动时出现更清晰的晚期峰值。这些时间段发生在约2 - 7分钟和15 - 40分钟，分别对应于所谓的1A期和1B期心律失常。只有晚高峰被视为触发交替。7.与使用非缺血心肌数据构建的曲线相比，缺血期间动作电位时程的电恢复曲线显示平台期进行性降低，幅度降低，并在1 h时变平。然而，在约15 - 45分钟时，下降出现逆转或减少。我们认为电交替是缺血心肌的一种独特的电生理特征，可能与室性心律失常和室颤有关，并且至少有两种机制有助于交替：（i）动作电位的电恢复和（ii）细胞内钙循环的变化。
1. Alternate long and short action potential durations, or electrical alternans, has only been sporadically observed in ischaemic myocardium in situ. We systematically studied alternans in the latter to characterize the phenomenon, relate it to ventricular arrhythmia and suggest possible mechanisms. 2. Sixteen Landrace pigs were anaesthetized (Azaperone, N2O and O2), ventilated and the hearts exposed. A branch of the left coronary artery was ligated. Left intraventricular and systemic pressures were monitored. Monophasic action potentials were recorded simultaneously with up to five suction electrodes in and around the proposed ischaemia area. 3. A computer measured the duration of every action potential, at several phases of repolarization, throughout the first hour of ischaemia. This allowed the systematic study of the alternans. Measurements during defined stimulus protocols were also made for the construction of electrical restitution curves. 4. Alternans was found in all recordings within the ischaemic area and in two‐thirds of those in the ‘border’ area. There was no alternans in non‐ischaemic areas. 5. The alternans, when action potential duration was plotted for every beat, appeared as an oscillation which was pleomorphic. It could be: (a) stable for hundreds of beats; (b) switched or triggered (by one extraneous beat having a different cycle length) between one stable state with high and one with low or absent alternans; (c) damped; (d) undamped to take a crescendo form, sometimes preceding ventricular fibrillation. 6. The alternans in general showed an ill‐defined peak incidence between about 200 to 1500 beats after the onset of ischaemia, and a clearer late peak at about 3000 beats. These periods occurred at about 2‐7 min and 15‐40 min, corresponding to so‐called phase 1A and 1B arrhythmia respectively. Only the late peak was seen with triggered alternans. 7. The electrical restitution curve for the action potential duration during ischaemia when compared with curves, constructed with data from non‐ischaemic myocardium, showed a progressive depression in plateau, a reduction in magnitude and was flattened at 1 h. However, there was a reversal or reduction in decline at about 15‐45 min. 8. We propose that electrical alternans is a distinctive electrophysiological characteristic of ischaemic myocardium which may be causally related to ventricular arrhythmia and fibrillation, and that at least two mechanisms contribute to the alternans: (i) electrical restitution of the action potential and (ii) changes in intracellular calcium cycling.