Department of Surgery, The University of Auckland, Auckland, New Zealand.
Neurogastroenterol Motil. 2012 Jul;24(7):e299-312. doi: 10.1111/j.1365-2982.2012.01932.x.
Gastric slow waves propagate aborally as rings of excitation. Circumferential propagation does not normally occur, except at the pacemaker region. We hypothesized that (i) the unexplained high-velocity, high-amplitude activity associated with the pacemaker region is a consequence of circumferential propagation; (ii) rapid, high-amplitude circumferential propagation emerges during gastric dysrhythmias; (iii) the driving network conductance might switch between interstitial cells of Cajal myenteric plexus (ICC-MP) and circular interstitial cells of Cajal intramuscular (ICC-IM) during circumferential propagation; and (iv) extracellular amplitudes and velocities are correlated.
An experimental-theoretical study was performed. High-resolution gastric mapping was performed in pigs during normal activation, pacing, and dysrhythmia. Activation profiles, velocities, and amplitudes were quantified. ICC pathways were theoretically evaluated in a bidomain model. Extracellular potentials were modeled as a function of membrane potentials.
High-velocity, high-amplitude activation was only recorded in the pacemaker region when circumferential conduction occurred. Circumferential propagation accompanied dysrhythmia in 8/8 experiments was faster than longitudinal propagation (8.9 vs 6.9 mm s(-1) ; P = 0.004) and of higher amplitude (739 vs 528 μV; P = 0.007). Simulations predicted that ICC-MP could be the driving network during longitudinal propagation, whereas during ectopic pacemaking, ICC-IM could outpace and activate ICC-MP in the circumferential axis. Experimental and modeling data demonstrated a linear relationship between velocities and amplitudes (P < 0.001).
CONCLUSIONS & INFERENCES: The high-velocity and high-amplitude profile of the normal pacemaker region is due to localized circumferential propagation. Rapid circumferential propagation also emerges during a range of gastric dysrhythmias, elevating extracellular amplitudes and organizing transverse wavefronts. One possible explanation for these findings is bidirectional coupling between ICC-MP and circular ICC-IM networks.
胃慢波呈环形兴奋波向头侧传播。除起搏区外,通常不会发生环形传播。我们假设:(i)起搏区与未解释的高速度、高幅度活动是环形传播的结果;(ii)在胃节律紊乱时出现快速、高幅度的环形传播;(iii)在环形传播过程中,起搏网络电导可能在平滑肌间 ICC (ICC-MP)和环形 ICC (ICC-IM)之间切换;(iv)细胞外幅度和速度是相关的。
进行了实验理论研究。在正常激活、起搏和节律紊乱期间,在猪中进行了高分辨率胃映射。量化了激活谱、速度和幅度。在双域模型中对 ICC 途径进行了理论评估。细胞外电势被建模为膜电势的函数。
当发生环形传导时,仅在起搏区记录到高速度、高幅度的激活。8/8 例节律紊乱时,环形传播速度快于纵向传播(8.9 与 6.9mm/s;P=0.004),幅度更高(739 与 528μV;P=0.007)。模拟预测,在纵向传播期间,ICC-MP 可能是起搏网络,而在异位起搏期间,ICC-IM 可以在环形轴上超过并激活 ICC-MP。实验和建模数据表明速度和幅度之间存在线性关系(P<0.001)。
正常起搏区的高速度和高幅度特征是由于局部环形传播所致。在多种胃节律紊乱中也会出现快速环形传播,从而提高细胞外幅度并组织横向波阵面。这些发现的一个可能解释是 ICC-MP 和环形 ICC-IM 网络之间的双向偶联。