THE ELECTROPHYSIOLOGY OF RABBIT HEARTS WITH LEFT-VENTRICULAR HYPERTROPHY UNDER NORMAL AND ISCHEMIC CONDITIONS

Objectives: To examine the cardiac electrophysiological effects of lef t ventricular hypertrophy (LVH) and to determine whether any observed differences are modified by global zero-flow ischaemia. Methods: LVH w as induced by perinephritic hypertension in New Zealand White rabbits. Transmembrane action potential recordings were made using conventiona l 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-mi n periods during ischaemia. Results: The post-operative blood pressure was 76(2) mmHg (mean(s.e.m.)) and 113(2) mmHg (P < 0.0005) in the sha m 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 e xhibited significant prolongations in action potential duration to 50% and 90% repolarisation (APD(50) APD(50)) and ERP of 20%, 12% and 19% respectively (P < 0.005) without any differences in resting membrane p otential (Em), upstroke velocity (dV/dt(max)) or amplitude (APA) of th e action potential. During ischaemia Em, APA and dV/dt(max) progressiv ely decreased to a similar extent in both groups. Ischaemia resulted i n shortenings in APD(50) APD(50) and ERP in the hypertrophy group of 1 22(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. Conclusions: There was enhanced shortening of APD and ventricul ar refractoriness in hypertrophied muscle during global ischaemia. Thi s could increase the dispersion of repolarization and refractoriness b etween normal and ischaemic hypertrophied muscle during regional ischa emia which may explain the increased susceptibility of hypertrophied h earts to arrhythmias.