Hancox J C, Mitcheson J S
Department of Physiology, School of Medical Science, University of Bristol, United Kingdom.
Can J Cardiol. 1997 Dec;13(12):1175-82.
To review findings from the authors' laboratory in studies of electrophysiological properties of single rod- and spindle-shaped myocytes from rabbit atrioventricular node (AVN).
Single cells were isolated from the AVN of the rabbit heart with the use of enzymatic and mechanical dispersion. For recording, cells were superfused with a Tyrode's solution at 33 to 37 degrees C, and recordings were made with microelectrodes or patch pipettes under 'current' or voltage' clamp conditions. Results are expressed as mean +/- SEM.
AVN cells had a mean membrane capacitance of 40 +/- 3.9 pF and membrane resistance of 565 +/- 167 M omega (n = 9). Spontaneously active cells exhibited pacemaker activity showing a clear diastolic depolarization and overshooting action potential (AP) with a relatively slow upstroke velocity (7.4 +/- 0.9 V/s, n = 6) and a maximum diastolic potential of -70.5 +/- 2.9 mV. Under voltage clamp conditions, depolarizing pulses from 40 mV elicited L-type calcium currents sensitive to inhibition by nifedipine and managanese or cadmium ions, which could also block spontaneous APs. Depolarizing pulses also activated delayed rectifier potassium current (IK). IK showed rapid activation, and IK 'tails' in AVN cells were blocked by 5 microM E4031, consistent with the rapidly activating subtype of IK (IKr). IK was similar in AVN and ventricular myocytes, except for the time-course of deactivation, which was faster in AVN cells. In 80% to 90% of cells, hyperpolarizing voltage steps activated a small time-independent current. Ten per cent to 20% of cells showed the hyperpolarization-activated current (I(f)), but I(f) amplitude was only significant at potentials more negative than the pacemaker potential. AVN cells showed an apparent absence of inwardly rectifying potassium current.
The high membrane resistance of AVN cells suggests that only small changes in ionic currents could significantly affect membrane potential. L-type calcium current is important in generating the AP upstroke, and IKr may play a role in both AP repolarization and diastolic depolarization. The ionic basis underlying spontaneous activity is not yet clear, but in some cells I(f) is not required because cells without I(f) can generate spontaneous APs.
回顾作者实验室对兔房室结（AVN）单个杆状和梭形心肌细胞电生理特性研究的结果。
采用酶解法和机械分散法从兔心脏的房室结分离单个细胞。记录时，细胞在33至37摄氏度下用台氏液灌流，并在“电流”或“电压”钳制条件下用微电极或膜片吸管进行记录。结果以平均值±标准误表示。
房室结细胞的平均膜电容为40±3.9 pF，膜电阻为565±167 MΩ（n = 9）。自发活动的细胞表现出起搏活动，呈现明显的舒张期去极化和超射动作电位（AP），上升速度相对较慢（7.4±0.9 V/s，n = 6），最大舒张电位为-70.5±2.9 mV。在电压钳制条件下，从-40 mV开始的去极化脉冲引发对硝苯地平、锰或镉离子抑制敏感的L型钙电流，这些离子也可阻断自发动作电位。去极化脉冲还激活延迟整流钾电流（IK）。IK表现出快速激活，房室结细胞中的IK“尾电流”被5 μM E4031阻断，这与IK的快速激活亚型（IKr）一致。IK在房室结和心室肌细胞中相似，只是失活的时间进程在房室结细胞中更快。在80%至90%的细胞中，超极化电压阶跃激活一个小的非时间依赖性电流。10%至20%的细胞表现出超极化激活电流（I(f)），但I(f)幅度仅在比起搏电位更负的电位时才显著。房室结细胞明显缺乏内向整流钾电流。
房室结细胞的高膜电阻表明离子电流的微小变化就可能显著影响膜电位。L型钙电流在动作电位上升支的产生中起重要作用，IKr可能在动作电位复极化和舒张期去极化中都起作用。自发活动背后的离子基础尚不清楚，但在一些细胞中不需要I(f)，因为没有I(f)的细胞也能产生自发动作电位。
