Sung Derrick, Mills Robert W, Schettler Jan, Narayan Sanjiv M, Omens Jeffrey H, McCulloch Andrew D
Department of Bioengineering, University of California San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0412, USA.
J Cardiovasc Electrophysiol. 2003 Jul;14(7):739-49. doi: 10.1046/j.1540-8167.2003.03072.x.
Mechanical stimulation can induce electrophysiologic changes in cardiac myocytes, but how mechanoelectric feedback in the intact heart affects action potential propagation remains unclear.
Changes in action potential propagation and repolarization with increased left ventricular end-diastolic pressure from 0 to 30 mmHg were investigated using optical mapping in isolated perfused rabbit hearts. With respect to 0 mmHg, epicardial strain at 30 mmHg in the anterior left ventricle averaged 0.040 +/- 0.004 in the muscle fiber direction and 0.032 +/- 0.006 in the cross-fiber direction. An increase in ventricular loading increased average epicardial activation time by 25%+/- 3% (P < 0.0001) and correspondingly decreased average apparent surface conduction velocity by 16%+/- 7% (P = 0.007). Ventricular loading did not significantly alter action potential duration at 20% repolarization (APD20) but did at 80% repolarization (APD80), from 179 +/- 7 msec to 207 +/- 5 msec (P < 0.0001). The dispersion of APD20 was decreased with loading from 19 +/- 2 msec to 13 +/- 2 msec (P = 0.024), whereas the dispersion of APD80 was not significantly changed. These electrophysiologic changes with ventricular loading were not affected by the nonspecific stretch-activated channel blocker streptomycin (200 microM) and were not attributable to changes in myocardial perfusion or the presence of an electromechanical decoupling agent (butanedione monoxime) during optical mapping.
Acute loading of the left ventricle of the isolated rabbit heart decreased apparent epicardial conduction velocity and increased action potential duration by a load-dependent mechanism that may not involve stretch-activated channels.
机械刺激可诱导心肌细胞发生电生理变化，但完整心脏中的机械电反馈如何影响动作电位的传播仍不清楚。
使用光学映射技术，研究了在离体灌注兔心脏中，随着左心室舒张末期压力从0 mmHg增加到30 mmHg，动作电位传播和复极化的变化。相对于0 mmHg，左心室前壁在30 mmHg时的心外膜应变在肌纤维方向平均为0.040±0.004，在横纤维方向平均为0.032±0.006。心室负荷增加使平均心外膜激活时间增加25%±3%（P<0.0001），相应地使平均表观表面传导速度降低16%±7%（P = 0.007）。心室负荷并未显著改变复极化20%时的动作电位时程（APD20），但在复极化80%时（APD80）有显著改变，从179±7毫秒增加到207±5毫秒（P<0.0001）。加载时APD20的离散度从19±2毫秒降低到13±2毫秒（P = 0.024），而APD80的离散度没有显著变化。这些心室负荷引起的电生理变化不受非特异性牵张激活通道阻滞剂链霉素（200 μM）的影响，也不归因于心肌灌注的变化或光学映射期间存在机电解耦剂（丁二酮单肟）。
离体兔心脏左心室的急性负荷通过一种可能不涉及牵张激活通道的负荷依赖性机制降低了表观心外膜传导速度并增加了动作电位时程。
