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心肌中的低传导性。生物物理模型。

Low conduction in cardiac muscle. Biophysical model.

作者信息

Lieberman M, Kootsey J M, Johnson E A, Sawanobori T

出版信息

Biophys J. 1973 Jan;13(1):37-55. doi: 10.1016/s0006-3495(73)85968-5.

Abstract

Mechanisms of slow conduction in cardiac muscle are categorized and the most likely identified. Propagating action potentials were obtained experimentally from a synthetically grown strand of cardiac muscle (around 50 mum by 30 mm) and theoretically from a one-dimensional cable model that incorporated varying axial resistance and membrane properties along its length. Action potentials propagated at about 0.3 m/s, but in some synthetic strands there were regions (approximately 100 mum in length) where the velocity decreased to 0.002 m/s. The electrophysiological behavior associated with this slow conduction was similar to that associated with slow conduction in naturally occurring cardiac muscle (notches, Wenckebach phenomena, and block). Theoretically, reasonable changes in specific membrane capacitance, membrane activity, and various changes in geometry were insufficient to account for the observed slow conduction velocities. Conduction velocities as low as 0.009 m/s, however, could be obtained by increasing the resistance (r(i)) of connections between the cells in the cable; velocities as low as 0.0005 m/s could be obtained by a further increase in r(i) made possible by a reduction in membrane activity by one-fourth, which in itself decreased conduction velocity by only a factor of 1/1.4. As a result of these findings, several of the mechanisms that have been postulated, previously, are shown to be incapable of accounting for delays such as those which occur in the synthetic strand as well as in the atrioventricular (VA) node.

摘要

心肌中缓慢传导的机制被分类并确定了最有可能的机制。通过实验从合成生长的心肌束(约50μm×30mm)中获取传播的动作电位,并从一维电缆模型中理论上获取,该模型沿其长度包含变化的轴向电阻和膜特性。动作电位以约0.3m/s的速度传播,但在一些合成束中存在区域(长度约100μm),其速度降至0.002m/s。与这种缓慢传导相关的电生理行为类似于与天然心肌中缓慢传导相关的行为(切迹、文氏现象和阻滞)。理论上,特定膜电容、膜活性的合理变化以及几何形状的各种变化不足以解释观察到的缓慢传导速度。然而,通过增加电缆中细胞间连接的电阻(r(i)),可以获得低至0.009m/s的传导速度;通过将膜活性降低四分之一使r(i)进一步增加,可以获得低至0.0005m/s的速度,而膜活性本身仅使传导速度降低1/1.4倍。这些发现的结果表明,先前假设的几种机制无法解释诸如在合成束以及房室(VA)节点中发生的延迟。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4184/1484178/225263587067/biophysj00715-0051-a.jpg

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