Kimura S, Bassett A L, Cameron J S, Huikuri H, Kozlovskis P L, Myerburg R J
Department of Medicine, University of Miami, School of Medicine, FL 33101.
Circulation. 1988 Aug;78(2):401-6. doi: 10.1161/01.cir.78.2.401.
Cellular electrophysiological consequences of acute ischemia superimposed on healed myocardial infarction were studied in isolated, coronary-perfused cat left ventricles 2-4 months after ligation of multiple distal tributaries of the left anterior descending and circumflex coronary arteries. Oxygenated Tyrode's solution was perfused through the left anterior descending and circumflex coronary arteries, and the preparations were superfused with Tyrode's solution gassed with 95% N2-5% CO2. Transmembrane action potentials were recorded from the endocardial cells in normal and infarcted zones. There were no significant differences in measured action potential variables and refractory periods between cells in the normal and infarcted zones before acute ischemia. When coronary perfusion was discontinued ("ischemia"), resting potential, action potential amplitude, and action potential duration were reduced, and the refractory period was shortened progressively in cells of the normal zone. However, the action potential changes were less prominent, and the refractory period was unchanged in cells in the infarcted zone. As a result, there were significant differences in resting membrane potential, action potential amplitude, action potential duration, and refractory period between cells in the normal and infarcted zones at 10 minutes of ischemia. These differences became larger as the ischemic period was prolonged. Spontaneous rapid ventricular activity was observed during the last 20-30 minutes of ischemia in four of eight preparations with healed myocardial infarction, whereas no spontaneous rapid ventricular activity was recorded in any of six normal heart preparations. Our data suggest that superimposition of acute ischemia on healed myocardial infarction produces electrophysiological inhomogeneities that may enhance arrhythmogenesis.
在结扎左冠状动脉前降支和左旋支的多个远端分支2 - 4个月后，对分离的、冠状动脉灌注的猫左心室进行研究，以探讨急性缺血叠加在愈合心肌梗死上的细胞电生理后果。通过左冠状动脉前降支和左旋支灌注含氧的台氏液，并用含95% N2 - 5% CO2的台氏液对标本进行 superfused（原文此处有误，推测为superfused）。记录正常区和梗死区心内膜细胞的跨膜动作电位。在急性缺血前，正常区和梗死区细胞的测量动作电位变量和不应期无显著差异。当冠状动脉灌注中断（“缺血”）时，正常区细胞的静息电位、动作电位幅度和动作电位时程降低，不应期逐渐缩短。然而，梗死区细胞的动作电位变化不太明显，不应期无变化。因此，在缺血10分钟时，正常区和梗死区细胞在静息膜电位、动作电位幅度、动作电位时程和不应期方面存在显著差异。随着缺血时间延长，这些差异变得更大。在八只愈合心肌梗死的标本中，有四只在缺血最后20 - 30分钟观察到自发性快速心室活动，而六只正常心脏标本中均未记录到自发性快速心室活动。我们的数据表明，急性缺血叠加在愈合心肌梗死上会产生电生理不均匀性，这可能会增强心律失常的发生。
