Eijsbouts Sabine C M, Houben Richard P M, Blaauw Yuri, Schotten Ulrich, Allessie Maurits A
Department of Physiology, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands.
J Cardiovasc Electrophysiol. 2004 Dec;15(12):1453-61. doi: 10.1046/j.1540-8167.2004.04326.x.
The aim of this study was to investigate the interaction of atrial dilation and blockade of the rapid sodium channel on atrial conduction and degree of anisotropy.
The right atrium was acutely dilated by increasing intra-atrial pressure from 2 to 9 cm H2O in 14 isolated rabbit hearts. A rectangular mapping array of 240 electrodes (spatial resolution 0.5 mm) was positioned on the free wall of the right atrium during pacing from four different directions at intervals of 240 and 140 msec. In nondilated atria, 0.5 and 1.0 mg/L of the use-dependent INa blocker flecainide prolonged the total conduction time under the mapping electrode by 15% to 75%. In dilated atria, flecainide depressed conduction by 24% to 89% (P < 0.05). The incidence of intra-atrial conduction block increased from 0.6%-0.8% to 3.3%-7.2% in nondilated atria and from 3.9%-4.6% to 13%-21% in dilated atria (P < 0.05). The direction of activation relative to the crista terminalis and major pectinate muscles was of major importance for occurrence of conduction block. During rapid pacing, the degree of anisotropy in conduction increased by the combination of atrial dilation and flecainide (1.0 mg/L) from 1.7 +/- 0.1 to 2.2 +/- 0.4 (P < 0.05). The effects of dilation and flecainide on conduction were clearly synergistic. The effect of flecainide on the atrial refractory period also was enhanced by atrial dilation.
In dilated atria, blockade of the rapid sodium channels caused a higher degree of local conduction delay and intra-atrial conduction block than in nondilated atria.
本研究旨在探讨心房扩张与快速钠通道阻滞剂对心房传导及各向异性程度的相互作用。
在14个离体兔心脏中，通过将心房内压力从2 cm H2O增加到9 cm H2O，使右心房急性扩张。在从四个不同方向以240和140毫秒的间隔进行起搏时，将一个由240个电极组成的矩形标测阵列（空间分辨率0.5毫米）置于右心房游离壁上。在未扩张的心房中，0.5和1.0毫克/升的使用依赖性钠通道阻滞剂氟卡尼使标测电极下的总传导时间延长了15%至75%。在扩张的心房中，氟卡尼使传导减慢24%至89%（P<0.05）。心房内传导阻滞的发生率在未扩张的心房中从0.6% - 0.8%增加到3.3% - 7.2%，在扩张的心房中从3.9% - 4.6%增加到13% - 21%（P<0.05）。相对于终嵴和主要梳状肌的激动方向对传导阻滞的发生至关重要。在快速起搏期间，心房扩张与氟卡尼（1.0毫克/升）联合作用使传导的各向异性程度从1.7±0.1增加到2.2±0.4（P<0.05）。扩张和氟卡尼对传导的影响明显具有协同作用。心房扩张也增强了氟卡尼对心房不应期的作用。
在扩张的心房中，快速钠通道的阻滞比在未扩张的心房中导致更高程度的局部传导延迟和心房内传导阻滞。
