Horner S M, Dick D J, Murphy C F, Lab M J
British Heart Foundation Cardiac Arrhythmia Research Group, Department of Physiology, Charing Cross and Westminster Medical School, London, UK.
Circulation. 1996 Sep 1;94(5):1131-6. doi: 10.1161/01.cir.94.5.1131.
Mechanoelectric feedback, the process by which changes in mechanical activity change the electrophysiology of the myocardium, has been linked to the genesis of arrhythmias. We investigated possible arrhythmogenic mechanisms by measuring changes in steady-state action potential duration and, more particularly, electrical restitution on a transiently applied load change, because action potential recovery may provide clues to arrhythmogenesis.
Pigs were anesthetized and their hearts exposed. A snare was placed around the aorta, and the right atrium was paced. Ventricular pressure, monophasic action potential, and segment motion were recorded from the left ventricle. The action potential duration was measured before and during transient aortic occlusion. Electrical restitution curves were constructed from the records obtained during normal loading or during transient aortic occlusion. The degree of shortening of action potential duration on aortic occlusion decreased with decreases in the steady-state beat-to-beat interval (P = .0008). Control restitution curves had the typical configuration, with a rapid initial, usually monotonic, rise toward a plateau. Some curves showed a marginal "supernormal" section. Increased load reduced the action potential duration at the plateau of the restitution curve (9.4 ms, P < .0001) but increased the action potential duration at the start of the restitution curve (8.7 ms, P = .03). Increased loading increased the maximum slope of the electrical restitution curve by 32 ms/100 ms (P = .04). Increased load also increased the supernormal period of the electrical restitution curves.
Mechanoelectric feedback produces changes in rate-dependent electrophysiology, which could favor a matrix conducive to arrhythmogenesis.
机械电反馈是指机械活动的变化改变心肌电生理学的过程，它与心律失常的发生有关。我们通过测量稳态动作电位时程的变化，尤其是在短暂施加负荷变化时的电恢复情况，来研究可能的致心律失常机制，因为动作电位恢复情况可能为心律失常的发生提供线索。
对猪进行麻醉并暴露心脏。在主动脉周围放置圈套器，并对右心房进行起搏。记录左心室的心室压力、单相动作电位和节段运动。在短暂主动脉阻断前后测量动作电位时程。根据正常负荷或短暂主动脉阻断期间获得的记录构建电恢复曲线。主动脉阻断时动作电位时程的缩短程度随着稳态逐搏间期的缩短而降低（P = 0.0008）。对照恢复曲线具有典型的形态，最初快速上升，通常呈单调上升趋势，直至达到平台期。一些曲线显示出轻微的“超常”部分。负荷增加会降低恢复曲线平台期的动作电位时程（9.4毫秒，P < 0.0001），但会增加恢复曲线起始处的动作电位时程（8.7毫秒，P = 0.03）。负荷增加使电恢复曲线的最大斜率增加32毫秒/100毫秒（P = 0.04）。负荷增加还会增加电恢复曲线的超常期。
机械电反馈会导致心率依赖性电生理学发生变化，这可能有利于形成易致心律失常的基质。
