Jongsma H J, Wilders R
Department of Medical Physiology, University Medical Center Utrecht, Utrecht, The Netherlands.
Circ Res. 2000 Jun 23;86(12):1193-7. doi: 10.1161/01.res.86.12.1193.
Connexins, the protein molecules forming gap junction channels, are reduced in number or redistributed from intercalated disks to lateral cell borders in a variety of cardiac diseases. This "gap junction remodeling" is considered to be arrhythmogenic. Using a simple model of human ventricular myocardium, we found that quantitative remodeling data extracted from the literature gave rise to only small to moderate changes in conduction velocity and the anisotropy ratio. Especially for longitudinal conduction, cytoplasmic resistivity (and thus cellular geometry) is much more important than commonly realized. None of the remodeling data gave rise to slow conduction on the order of a few centimeters per second.
构成缝隙连接通道的蛋白质分子——连接蛋白，在多种心脏疾病中数量减少或从闰盘重新分布到细胞侧面边界。这种“缝隙连接重塑”被认为是致心律失常的。通过一个简单的人类心室心肌模型，我们发现从文献中提取的定量重塑数据仅导致传导速度和各向异性比率出现小到中度的变化。特别是对于纵向传导，细胞质电阻率（以及细胞几何形状）比通常认为的要重要得多。没有任何重塑数据会导致每秒几厘米量级的缓慢传导。
