Department of Physiology, University of Bern, Bern, Switzerland.
Laboratory for Soft Bioelectronic Interfaces, EPFL, Geneva, Switzerland.
J Physiol. 2022 Jul;600(14):3287-3312. doi: 10.1113/JP283083. Epub 2022 Jun 23.
Cardiomyocyte cultures exhibit spontaneous electrical and contractile activity, as in a natural cardiac pacemaker. In such preparations, beat rate variability exhibits features similar to those of heart rate variability in vivo. Mechanical deformations and forces feed back on the electrical properties of cardiomyocytes, but it is not fully elucidated how this mechano-electrical interplay affects beating variability in such preparations. Using stretchable microelectrode arrays, we assessed the effects of the myosin inhibitor blebbistatin and the non-selective stretch-activated channel blocker streptomycin on beating variability and on the response of neonatal or fetal murine ventricular cell cultures against deformation. Spontaneous electrical activity was recorded without stretch and upon predefined deformation protocols (5% uniaxial and 2% equibiaxial strain, applied repeatedly for 1 min every 3 min). Without stretch, spontaneous activity originated from the edge of the preparations, and its site of origin switched frequently in a complex manner across the cultures. Blebbistatin did not change mean beat rate, but it decreased the spatial complexity of spontaneous activity. In contrast, streptomycin did not exert any manifest effects. During the deformation protocols, beat rate increased transiently upon stretch but, paradoxically, also upon release. Blebbistatin attenuated the response to stretch, whereas this response was not affected by streptomycin. Therefore, our data support the notion that in a spontaneously firing network of cardiomyocytes, active force generation, rather than stretch-activated channels, is involved mechanistically in the complexity of the spatiotemporal patterns of spontaneous activity and in the stretch-induced acceleration of beating. KEY POINTS: Monolayer cultures of cardiac cells exhibit spontaneous electrical and contractile activity, as in a natural cardiac pacemaker. Beating variability in these preparations recapitulates the power-law behaviour of heart rate variability in vivo. However, the effects of mechano-electrical feedback on beating variability are not yet fully understood. Using stretchable microelectrode arrays, we examined the effects of the contraction uncoupler blebbistatin and the non-specific stretch-activated channel blocker streptomycin on beating variability and on stretch-induced changes of beat rate. Without stretch, blebbistatin decreased the spatial complexity of beating variability, whereas streptomycin had no effects. Both stretch and release increased beat rate transiently; blebbistatin attenuated the increase of beat rate upon stretch, whereas streptomycin had no effects. Active force generation contributes to the complexity of spatiotemporal patterns of beating variability and to the increase of beat rate upon mechanical deformation. Our study contributes to the understanding of how mechano-electrical feedback influences heart rate variability.
心肌细胞培养物表现出自发的电和收缩活动,就像天然心脏起搏器一样。在这些制剂中,心率变异性的变化率表现出与体内心率变异性相似的特征。机械变形和力反馈到心肌细胞的电特性上,但尚不完全清楚这种力学-电学相互作用如何影响这些制剂中的搏动变异性。使用可拉伸微电极阵列,我们评估了肌球蛋白抑制剂 blebbistatin 和非选择性张力激活通道阻滞剂链霉素对搏动变异性以及对变形反应的新生或胎儿鼠心室细胞培养物的影响。在没有拉伸的情况下记录自发的电活动,并在预定义的变形方案(5%单轴和 2%等双轴应变,每 3 分钟重复施加 1 分钟)下记录。在没有拉伸的情况下,自发活动起源于制剂的边缘,其起源点在整个培养物中以复杂的方式频繁切换。Blebbistatin 没有改变平均跳动率,但它降低了自发活动的空间复杂性。相比之下,链霉素没有产生任何明显的影响。在变形方案中,跳动率在拉伸时短暂增加,但矛盾的是,在释放时也增加。Blebbistatin 减弱了对拉伸的反应,而这种反应不受链霉素的影响。因此,我们的数据支持这样的观点,即在自发放电的心肌细胞网络中,主动力生成而不是张力激活通道,在空间和时间模式的自发性活动复杂性以及拉伸诱导的跳动加速中涉及机械作用。要点:心脏细胞的单层培养物表现出自发的电和收缩活动,就像天然心脏起搏器一样。这些制剂中的跳动变异性再现了体内心率变异性的幂律行为。然而,机械电反馈对跳动变异性的影响尚不完全清楚。使用可拉伸微电极阵列,我们检查了收缩偶联剂 blebbistatin 和非特异性张力激活通道阻滞剂链霉素对跳动变异性和拉伸诱导的跳动率变化的影响。在没有拉伸的情况下,blebbistatin 降低了跳动变异性的空间复杂性,而链霉素没有影响。拉伸和释放都会使跳动率短暂增加;blebbistatin 减弱了拉伸时跳动率的增加,而链霉素没有影响。主动力生成有助于跳动变异性的时空模式的复杂性以及机械变形时跳动率的增加。我们的研究有助于理解机械电反馈如何影响心率变异性。