Näbauer M, Beuckelmann D J, Erdmann E
Department of Medicine I, University of Munich, Germany.
Circ Res. 1993 Aug;73(2):386-94. doi: 10.1161/01.res.73.2.386.
A variety of outward currents exists in ventricular myocardium of different species influencing action potential duration and electrical activity. Transient outward currents have been reported in ventricular tissue of some animals but are small or absent in others. This study was conducted to investigate whether a transient outward current exists in human ventricular myocardium and to characterize its basic electrophysiological properties. Currents were recorded from enzymatically isolated human ventricular myocytes obtained from explanted hearts of 22 patients with terminal heart failure. In almost all cells studied, a transient outward current could be recorded on depolarization to between -20 and +80 mV. The size of the transient outward current was usually large enough to mask the Ca2+ current. It could be recorded under conditions in which Ca2+ influx and intracellular Ca2+ transients were suppressed. Basic current characteristics were similar to transient outward currents observed in other species. Inactivation of the transient outward current was monoexponential, with a time constant of 54.8 +/- 3.7 milliseconds at +40 mV. Half-maximal activation occurred at 16.7 +/- 1.6 mV; half-maximal steady-state inactivation occurred at -34.5 +/- 2.3 mV. Frequency-dependent reduction of peak transient outward current was 29.8 +/- 1.4% at 2 Hz compared with resting conditions. Recovery from inactivation was voltage dependent and had a biexponential time course; the faster time constant (41.0 +/- 6.5 milliseconds at -80 mV) accounted for 86.0 +/- 5.2% of total current. The transient outward current was sensitive to 4-aminopyridine (IC50, 1.15 mM). These results indicate that a large Ca(2+)-independent transient outward K+ current is present in human ventricular myocytes that might be regulated by physiological or pathological events and is a potential site for pharmacological intervention.
不同物种的心室肌中存在多种外向电流,这些电流会影响动作电位持续时间和电活动。在一些动物的心室组织中已报道存在瞬时外向电流,但在其他动物中则较小或不存在。本研究旨在调查人类心室肌中是否存在瞬时外向电流,并表征其基本电生理特性。从22例终末期心力衰竭患者的离体心脏中获取的酶解分离的人类心室肌细胞记录电流。在几乎所有研究的细胞中,去极化至-20至+80 mV之间时均可记录到瞬时外向电流。瞬时外向电流的大小通常足以掩盖Ca2+电流。在Ca2+内流和细胞内Ca2+瞬变受到抑制的条件下也可记录到该电流。基本电流特征与在其他物种中观察到的瞬时外向电流相似。瞬时外向电流的失活是单指数的,在+40 mV时时间常数为54.8±3.7毫秒。半数最大激活发生在16.7±1.6 mV;半数最大稳态失活发生在-34.5±2.3 mV。与静息状态相比,在2 Hz时峰值瞬时外向电流的频率依赖性降低为29.8±1.4%。失活后的恢复是电压依赖性的,具有双指数时间进程;较快的时间常数(在-80 mV时为41.0±6.5毫秒)占总电流的86.0±5.2%。瞬时外向电流对4-氨基吡啶敏感(IC50,1.15 mM)。这些结果表明,人类心室肌细胞中存在一种大的非Ca2+依赖性瞬时外向K+电流,该电流可能受生理或病理事件调节,是药物干预的潜在靶点。