Hicks M N, McIntosh M A, Kane K A, Rankin A C, Cobbe S M
Department of Medical Cardiology, Royal Infirmary, Glasgow, UK.
Cardiovasc Res. 1995 Aug;30(2):181-6.
To examine the cardiac electrophysiological effects of left ventricular hypertrophy (LVH) and to determine whether any observed differences are modified by global zero-flow ischaemia.
LVH was induced by perinephritic hypertension in New Zealand White rabbits. Transmembrane action potential recordings were made using conventional floating glass microelectrodes and effective refractory periods (ERP) determined by programmed stimulation in isolated arterially perfused interventricular septa during normal perfusion and a 30-min period of global ischaemia. The electrophysiological data were pooled into 6-min periods during ischaemia.
The post-operative blood pressure was 76(2) mmHg (mean(s.e.m.)) and 113(2) mmHg (P < 0.0005) in the sham and perinephritic rabbits respectively. The left ventricular to body weight ratio was 0.27(0.01) g kg-1 in the sham and 0.36(0.02) g kg-1 in the perinephritic group (P < 0.005) representing 33% hypertrophy. In the isolated septa, prior to ischaemia, the hypertrophied group exhibited significant prolongations in action potential duration to 50% and 90% repolarisation (APD50, APD90) and ERP of 20%, 12% and 19% respectively (P < 0.005) without any differences in resting membrane potential (Em), upstroke velocity (dV/dtmax) or amplitude (APA) of the action potential. During ischaemia Em, APA and dV/dtmax progressively decreased to a similar extent in both groups. Ischaemia resulted in shortenings in APD50, APD90 and ERP in the hypertrophy group of 122(9) ms, 131(8) ms and 99 (6) ms respectively which were greater than those observed in the control group (84 (7) ms, 115 (7) ms and 50 (13) ms, P < 0.05). These differences resulted in loss of the preischaemic prolongation of repolarisation and refractoriness in the hypertrophy group.
There was enhanced shortening of APD and ventricular refractoriness in hypertrophied muscle during global ischaemia. This could increase the dispersion of repolarization and refractoriness between normal and ischaemic hypertrophied muscle during regional ischaemia which may explain the increased susceptibility of hypertrophied hearts to arrhythmias.
研究左心室肥厚（LVH）的心脏电生理效应，并确定整体零流量缺血是否会改变所观察到的任何差异。
通过肾周高血压诱导新西兰白兔发生左心室肥厚。使用传统的漂浮玻璃微电极记录跨膜动作电位，并在正常灌注和30分钟整体缺血期间，通过程控刺激在离体动脉灌注的室间隔中测定有效不应期（ERP）。缺血期间的电生理数据按6分钟时间段进行汇总。
假手术组和肾周高血压组术后血压分别为76（2）mmHg（平均值（标准误））和113（2）mmHg（P<0.0005）。假手术组左心室与体重比为0.27（0.01）g·kg⁻¹，肾周高血压组为0.36（0.02）g·kg⁻¹（P<0.005），代表33%的肥厚。在离体室间隔中，缺血前，肥厚组动作电位持续时间至复极化50%和90%（APD50、APD90）以及ERP分别显著延长20%、12%和19%（P<0.005），静息膜电位（Em）、动作电位上升速度（dV/dtmax）或幅度（APA）无差异。缺血期间，两组的Em、APA和dV/dtmax均逐渐下降至相似程度。缺血导致肥厚组的APD50、APD90和ERP分别缩短122（9）ms、131（8）ms和99（6）ms，大于对照组观察到的缩短程度（84（7）ms、115（7）ms和50（13）ms，P<0.05）。这些差异导致肥厚组缺血前复极化和不应期延长消失。
整体缺血期间，肥厚心肌的动作电位时程和心室不应期缩短增强。这可能会增加局部缺血期间正常心肌和缺血性肥厚心肌之间复极化和不应期的离散度，这可能解释了肥厚心脏对心律失常易感性增加的原因。
