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首页> 外文期刊>Progress in Biophysics and Molecular Biology: An International Review Journal >Experimental and computational studies of strain-conduction velocity relationships in cardiac tissue.
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Experimental and computational studies of strain-conduction velocity relationships in cardiac tissue.

机译：心脏组织中应变传导速度关系的实验和计算研究。

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Velocity of electrical conduction in cardiac tissue is a function of mechanical strain. Although strain-modulated velocity is a well established finding in experimental cardiology, its underlying mechanisms are not well understood. In this work, we summarized potential factors contributing to strain-velocity relationships and reviewed related experimental and computational studies. We presented results from our experimental studies on rabbit papillary muscle, which supported a biphasic relationship of strain and velocity under uni-axial straining conditions. In the low strain range, the strain-velocity relationship was positive. Conduction velocity peaked with 0.59 m/s at 100% strain corresponding to maximal force development. In the high strain range, the relationship was negative. Conduction was reversibly blocked at 118+/-1.8% strain. Reversible block occurred also in the presence of streptomycin. Furthermore, our studies revealed a moderate hysteresis of conduction velocity, which was reduced by streptomycin. We reconstructed several features of the strain-velocity relationship in a computational study with a myocyte strand. The modeling included strain-modulation of intracellular conductivity and stretch-activated cation non-selective ion channels. The computational study supported our hypotheses, that the positive strain-velocity relationship at low strain is caused by strain-modulation of intracellular conductivity and the negative relationship at high strain results from activity of stretch-activated channels. Conduction block was not reconstructed in our computational studies. We concluded this work by sketching a hypothesis for strain-modulation of conduction and conduction block in papillary muscle. We suggest that this hypothesis can also explain uni-axially measured strain-conduction velocity relationships in other types of cardiac tissue, but apparently necessitates adjustments to reconstruct pressure or volume related changes of velocity in atria and ventricles.
机译：心脏组织中的电传导速度是机械应变的函数。尽管应变调制速度是实验心脏病学中一个公认的发现，但其潜在机制尚不清楚。在这项工作中，我们总结了有助于应变-速度关系的潜在因素，并回顾了相关的实验和计算研究。我们提出了对兔乳头肌的实验研究结果，该结果支持了单轴应变条件下应变与速度的双相关系。在低应变范围内，应变-速度关系为正。传导速度在100％应变下达到0.59 m / s的峰值，对应于最大力的发展。在高应变范围内，该关系为负。在118 +/- 1.8％应变下可逆地阻止了传导。在链霉素的存在下也发生可逆性阻滞。此外，我们的研究表明，传导速度有中等程度的滞后，而链霉素可降低这种滞后。我们在与肌细胞链的计算研究中重建了应变-速度关系的几个特征。建模包括细胞内电导率和拉伸激活阳离子非选择性离子通道的应变调节。计算研究支持了我们的假设，即低应变时的正应变-速度关系是由细胞内电导率的应变调制引起的，而高应变时的负关系是由拉伸激活通道的活动引起的。传导阻滞未在我们的计算研究中重建。我们通过勾勒乳头肌传导和传导阻滞的应变调节假说来结束这项工作。我们建议，该假设还可以解释其他类型的心脏组织中单轴测量的应变传导速度关系，但显然需要进行调整以重建与心房和心室中压力或体积相关的速度变化。

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