Kodama I, Shibata N, Sakuma I, Mitsui K, Iida M, Suzuki R, Fukui Y, Hosoda S, Toyama J
Department of Circulation, Nagoya University, Japan.
Am J Physiol. 1994 Jul;267(1 Pt 2):H248-58. doi: 10.1152/ajpheart.1994.267.1.H248.
To clarify the mechanisms underlying cardiac dysfunction after electrical defibrillation, we investigated the effects of direct current field stimulation (10 ms, 1-80 V/cm) on isolated guinea pig papillary muscles. Shocks (S2) > 15 V/cm lowered the plateau height of the S2-induced action potential and inhibited its terminal repolarization. Subsequent responses to basic stimuli (S1, 1.0 Hz) for 1-3 min were characterized by a decrease in the maximum diastolic potential, a shortening of action potential duration, and an increase of the developed tension. With S2 > 30 V/cm, a marked delay in repolarization of the S2-induced action potential was followed by oscillation of membrane potential, resulting in repetitive spontaneous activity and often refractoriness to S1 stimulation. The aftereffects were independent of the phase of S2 application. Most of the aftereffects were preserved in the presence of nifedipine (1 microM) or ryanodine (1 microM). Only sodium channel blockade by tetrodotoxin (10 microM) modified the aftereffects by depressing the generation of spontaneous activity. These findings suggest that strong shocks (> 15 V/cm) will produce abnormal arrhythmogenic responses probably through a transient rupture of sarcolemmal membrane (electroporation) leading to a disturbance of the ionic equilibrium of the myocyte.
为阐明电除颤后心脏功能障碍的潜在机制，我们研究了直流电场刺激（10毫秒，1 - 80伏/厘米）对离体豚鼠乳头肌的影响。强度大于15伏/厘米的电击（S2）会降低S2诱导动作电位的平台期高度，并抑制其终末复极化。随后对基础刺激（S1，1.0赫兹）持续1 - 3分钟的反应表现为最大舒张电位降低、动作电位时程缩短以及张力增加。当S2大于30伏/厘米时，S2诱导动作电位的复极化明显延迟，随后膜电位振荡，导致重复性自发活动，且常对S1刺激产生不应性。这些后效应与施加S2的相位无关。在硝苯地平（1微摩尔）或ryanodine（1微摩尔）存在的情况下，大部分后效应得以保留。只有河豚毒素（10微摩尔）阻断钠通道通过抑制自发活动的产生来改变后效应。这些发现表明，强电击（大于15伏/厘米）可能通过肌膜的短暂破裂（电穿孔）导致心肌细胞离子平衡紊乱，从而产生异常的致心律失常反应。
