DIFFERENCES IN RATE DEPENDENCE OF TRANSIENT OUTWARD CURRENT IN RABBIT AND HUMAN ATRIUM
DIFFERENCES IN RATE DEPENDENCE OF TRANSIENT OUTWARD CURRENT IN RABBIT AND HUMAN ATRIUM
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DOI：
10.1152/ajpheart.1992.263.6.h1747
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发表时间：
1992-12-01
影响因子：
--
通讯作者：
NATTEL, S
中科院分区：
文献类型：
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作者：
FERMINI, B;WANG, Z;NATTEL, S
人和兔心房细胞都具有较大的4-氨基吡啶敏感瞬态外向电流（I(to1)）。然而，这种电流在兔子体内的缓慢再激活表明，它的作用可能仅限于非常慢的心率。我们用全细胞电压钳记录法评价兔和人心房肌细胞I（to1）的速率依赖性。我们的研究结果表明，在人体心房的生理温度下，I（to1）在0.1和4.0 Hz之间的速率无关。兔4.0 Hz的峰值I（to1）为0.1 Hz电流的3.4 +/- 1.4%（平均+/- SE） （P < 0.001, n = 8），而人4.0 Hz的峰值I（to1）平均为0.1 Hz电流的88.8 +/- 6.1% （P < 0.05, n = 7）。这些差异是由于再激活时间过程的显着差异，兔（n = 8）的双指数时间常数平均为650 +/- 159 ms和8.4 +/- 1.1 s，而人类心房（均为30℃）的单指数时间常数为33.6 +/- 6.8 ms （n = 8）。这些发现表明，I（to1）对人类所有生理心率下的心房复极都有重要作用。此外，这些结果强调，在I（to1）的速率依赖性方面存在重要的种间差异，这在理解心房复极的生理和药理调节时需要考虑。
Both human nd rabbit atrial cells possess a large 4-aminopyridine-sensitive transient outward current (I(to1)). However, the slow reactivation of this current in rabbits suggests that its role may be limited to very slow heart rates. We used whole cell voltage-clamp recordings to evaluate the rate dependency of I(to1) in rabbit and human atrial myocytes. Our results show that at physiological temperatures in human atrium, I(to1) is rate independent at rates between 0.1 and 4.0 Hz. Peak I(to1) at 4.0 Hz in rabbit was 3.4 +/- 1.4% (mean +/- SE) of current at 0.1 Hz (P < 0.001, n = 8), whereas in humans, peak I(to1) at 4.0 Hz averaged 88.8 +/- 6.1% of the current at 0.1 Hz (P > 0.05, n = 7). These differences were due to marked discrepancies in reactivation time course, which was biexponential with time constants that averaged 650 +/- 159 ms and 8.4 +/- 1.1 s in rabbit (n = 8) compared with a single exponential time constant of 33.6 +/- 6.8 ms (n = 8) in human atrium (both at 30-degrees-C). These findings suggest that I(to1) can contribute importantly to atrial repolarization at all physiological heart rates in humans. Furthermore, these results emphasize that there are important interspecies variations in the rate dependence of I(to1), which need to be considered in understanding the physiological and pharmacological regulation of atrial repolarization.