Dick D J, Lab M J
Department of Physiology, Charing Cross and Westminster Medical School, London, UK.
Cardiovasc Res. 1998 Apr;38(1):181-91. doi: 10.1016/s0008-6363(97)00314-3.
Mechanoelectric Feedback, a mechanical intervention inducing an electrical change, is gaining credence as a cause of cardiac arrhythmia in the clinical situation. However, the precise mechanism is unknown. To elucidate this we investigated mechanical and chemical modulation of stretch-induced premature ventricular beats.
We positioned a balloon in the left ventricle of an isolated heart (New Zealand White rabbit), perfused by the Langendorff technique. Balloon inflation regularly produces premature ventricular beats. Monophasic action potentials, ECG's and pressure recordings monitored changes, during mechanical intervention. The hearts were subjected to (i) variations in the degree of preload and duration of inflation, and (ii) cytoskeletal disrupters, colchicine and cytochalasin-B.
Mechanical dilation of the left ventricle can not only induce premature ventricular beats, but also induce a period during which premature beats cannot be re-induced on a subsequent inflation, i.e. a mechanoelectric adaptation period. The trigger for the mechanoelectric adaptation period seems to occur immediately on balloon inflation and required up to 60 s to recover. This period started with an undershoot in the diastolic component of the monophasic action potential as well as in the peak systolic pressure, with return to control levels within the period. Deflation produced an overshoot (rather than undershoot) in the monophasic action potential duration, but this also returned to control levels within the period. Changes in preload, duration of inflation and disruption of the cytoskeleton failed to modulate the mechanically induced premature beats, or the mechanoelectric adaptation period.
Transient ventricular stretch produces arrhythmia, followed by an antiarrhythmic adaptive period. Possible mechanisms are related to a mechanical influence on stretch-activated channels, changes in ionic concentration or diffusion, or second messenger systems, which influence membrane potential. The arrhythmic adaptation does not appear to be related to the mechanical properties of the cytoskeleton. Final elucidation of the mechanism of the mechanoelectric adaptation period demonstrated, may prove important in determining the mechanism of stretch-induced premature ventricular beats and consequently arrhythmia management.
机械电反馈是一种引起电变化的机械干预，在临床情况下作为心律失常的一个病因正逐渐得到认可。然而，其确切机制尚不清楚。为阐明这一点，我们研究了牵张诱导的室性早搏的机械和化学调节。
我们将一个球囊置于离体心脏（新西兰白兔）的左心室内，采用Langendorff技术进行灌注。球囊充气会定期产生室性早搏。在机械干预期间，单相动作电位、心电图和压力记录监测变化。对心脏进行（i）前负荷程度和充气持续时间的变化，以及（ii）细胞骨架破坏剂秋水仙碱和细胞松弛素-B处理。
左心室的机械扩张不仅可诱发室性早搏，还可诱发一个在随后充气时不能再次诱发早搏的时期，即机械电适应期。机械电适应期的触发似乎在球囊充气时立即发生，需要长达60秒才能恢复。这个时期开始时，单相动作电位的舒张期成分以及收缩压峰值出现下冲，并在该时期内恢复到对照水平。放气使单相动作电位持续时间出现上冲（而非下冲），但这也在该时期内恢复到对照水平。前负荷、充气持续时间的变化以及细胞骨架的破坏未能调节机械诱导的早搏或机械电适应期。
短暂的心室牵张会产生心律失常，随后出现抗心律失常的适应期。可能的机制与对牵张激活通道的机械影响、离子浓度或扩散的变化或第二信使系统有关，这些会影响膜电位。心律失常的适应似乎与细胞骨架的机械特性无关。最终阐明所证明的机械电适应期的机制，可能对确定牵张诱导的室性早搏的机制以及因此的心律失常管理具有重要意义。
