Yamamoto M, Honjo H, Niwa R, Kodama I
Department of Humoral Regulation, Nagoya University, Japan.
Cardiovasc Res. 1998 Aug;39(2):360-72. doi: 10.1016/s0008-6363(98)00091-1.
To study the morphology of small extracellular potentials localized to the sinoatrial (SA) node and to elucidate its potential usefulness in evaluating SA node dysfunction.
Extracellular potentials were recorded from the endocardial surface of the SA node in isolated right atrial preparations of rabbits through custom-made modified bipolar electrodes with high-gain amplification and a low-frequency (0.5-32 Hz) filter setting.
The potentials in and around the SA node under control conditions showed a variety of morphologies. In a small area near the leading pacemaker site, slow primary negative deflections were preceded by a gradual increase of the negativity (73.5 +/- 5.6 microV in amplitude, n = 12). In the periphery of the SA node cranial and caudal to the leading pacemaker site, slow positive/negative deflections were recorded. In the septal side of the SA node showing very slow conduction, the electrograms showed slow primary positive deflections. Transient pacemaker shifts induced by atrial stimulation or vagal nerve stimulation were reflected well in morphologies of the extracellular potentials. In the presence of 20 microM TTX, wide and slow negative deflections were observed in the center and periphery of the SA node in association with extremely slow conduction restricted to a corridor-like area along the crista terminalis, whereas the atrial muscle surrounding the area was made inexcitable. In the presence of 1 microM nifedipine, the leading pacemaker site was shifted to the periphery of the SA node close to the crista terminalis. The negative deflection in the center and septal side of the SA node disappeared reflecting no excitation of the area.
The endocardial extracellular electrograms recorded in and around the SA node under appropriate conditions reflect two dimensional activation sequences. They would provide useful information in recognizing the leading pacemaker site and alterations of the conductivity and excitability.
研究局限于窦房(SA)结的小细胞外电位的形态,并阐明其在评估窦房结功能障碍方面的潜在用途。
通过定制的改良双极电极,在高增益放大和低频(0.5 - 32 Hz)滤波设置下,从兔离体右心房标本的窦房结心内膜表面记录细胞外电位。
对照条件下窦房结及其周围的电位呈现出多种形态。在主导起搏点附近的小区域,缓慢的原发性负向偏转之前有负性逐渐增加(幅度为73.5 ± 5.6 μV,n = 12)。在主导起搏点头侧和尾侧的窦房结周边,记录到缓慢的正/负向偏转。在窦房结间隔侧显示传导非常缓慢,电图显示缓慢的原发性正向偏转。心房刺激或迷走神经刺激引起的短暂起搏点移位在细胞外电位形态中得到很好的反映。在存在20 μM 河豚毒素(TTX)的情况下,在窦房结中心和周边观察到宽而缓慢的负向偏转,同时传导极其缓慢,局限于沿终嵴的类似走廊的区域,而该区域周围的心房肌变得不可兴奋。在存在1 μM硝苯地平的情况下,主导起搏点转移到靠近终嵴的窦房结周边。窦房结中心和间隔侧的负向偏转消失,反映该区域无兴奋。
在适当条件下记录的窦房结及其周围的心内膜细胞外电图反映了二维激活序列。它们将为识别主导起搏点以及传导性和兴奋性的改变提供有用信息。