Nilius B, Boldt W, Scheufler K
Biomed Biochim Acta. 1984;43(1):101-10.
Afterpotentials following a train of paced action potentials in isolated pectinate muscles bordering the crista terminalis in the rabbit atrial myocardium were analyzed. Electrical measurements were performed using a standard microelectrode technique. An ultrastructural stereological analysis was undertaken to study intercellular clefts within the preparations used. After cessation of a rapid drive, afterpotentials showed an initial depolarization followed by a delayed hyperpolarization. The initial depolarization could be blocked by verapamil (13.2 microM) leaving a monotonous hyperpolarization. This hyperpolarization was modelled supposing a K+-depletion out of morphological identified intercellular clefts. From best approximation of the measured after-hyperpolarization (1) the internal K+ activity was estimated to be in the range of 82 to 90 mM depending on the pacing interval Io. It decreased due to shortening of Io; (2) the accumulated "cleft" K+ activity was estimated to be about 2 mM at a pre-drive pacing interval of 250 ms; it decreased by increasing of Io, (3) decreasing of Io accelerated the K+-depletion, (4) a single beat accumulation of about 0.28 mM was estimated. The morphologically measured geometry of the intercellular clefts (mean cleft width 0.5 micron, ratio of cleft and cell volume 0.09 +/- 0.03) agreed well with the electrophysiological findings.
对兔心房心肌终嵴边缘分离的梳状肌中一串起搏动作电位后的后电位进行了分析。使用标准微电极技术进行电测量。进行了超微结构立体分析,以研究所用制剂中的细胞间缝隙。快速驱动停止后,后电位显示出初始去极化,随后是延迟的超极化。维拉帕米(13.2微摩尔)可阻断初始去极化,仅留下单调的超极化。假设从形态学确定的细胞间缝隙中耗尽钾离子,对这种超极化进行了建模。根据测量的超极化后的最佳近似值:(1)根据起搏间隔Io,估计内部钾离子活性在82至90毫摩尔范围内。它因Io缩短而降低;(2)在驱动前起搏间隔为250毫秒时,累积的“缝隙”钾离子活性估计约为2毫摩尔;它因Io增加而降低,(3)Io减小加速了钾离子耗尽,(4)估计单次搏动积累约0.28毫摩尔。细胞间缝隙的形态学测量几何形状(平均缝隙宽度0.5微米,缝隙与细胞体积比0.09±0.03)与电生理结果吻合良好。