Effects of atrial natriuretic peptide on abnormal automaticity of diseased human atrial muscles.

人心房小梁（0.8xl）。从接受心脏手术的患者切除的一小块右心耳上剥离。我们首先尝试用双管K^+-和Na^+敏感微电极阐明人类心房制剂低静息膜电位（Vm）的离子机制。因为在标本中观察到的各种类型的异常自动性约占70%，可能主要是由Vm的部分去极化引起的。细胞内K^+活性（a^i_平均99.7<正负>1.3mM(n=33)），细胞内Na^+活性（a^i_, 6.9<正负>1.7mM(n=9)）和Vm， 43.6<正负>3.2（n=42）。这些发现表明Vm的去极化既不是由于a^i_的减少也不是由于a^i_的增加，而可能是由于膜K^+通透性的降低。其次，我们研究了心房钠肽（ANP）对人体制剂的动作电位特征和收缩张力的影响。然而，我们发现ANP对这些参数没有显著影响。因此，我们拟采用全细胞电压箝位技术检测ANP对单个心房肌细胞离子电流的影响。然而，在31个进行细胞分离的人心房组织中，只有一个分离细胞可以进行实验。因此，虽然我们观察到乙酰胆碱和尼可地尔对单个心房细胞的电生理作用是合理的，但我们无法获得ANP对单个心房细胞电生理作用的可用信息。

A human atrial trabecula(0.8xl. 5mm)was dissected from a small piece of right atrial appendage excised from patients undergoing cardiac surgery. We first attempted to elucidate the ionic mechanisms for the low resting membrane potential(Vm)of human atrial preparations using double-barreled K^+- and Na^+-sensitive microelectrodes. Because various types of abnormal automaticities observed at a rate of about 70% in the ppecimens may be mainly caused by partial depolarizations of Vm. The intracellular K^+ activity(a^i_averaged 99.7<plus-minus>1.3mM(n=33), intracellular Na^+ activity(a^i_, 6.9<plus-minus>1.7mM(n=9)and Vm, 43.6<plus-minus>3.2(n=42). These findings suggest that the depolarization of Vm is neither due to a decrease in a^i_ nor an increase in a^i_ but probably due to a decrease in K^+ permeability for the membrane. We secondly examined the effects of atrial natriuretic peptide(ANP)on action potential characteristics and contractile tension of the human preparations. However, we found no significant effect of ANP on those parameters. So we intended to test the effects of ANP on the ionic current in single human atrial myocytes using whole cell voltage-clamp technique. However, there was only one isolated cell tolerable to do experiment among 31 human atrial tissues undergone cell-isolation procedures. Therefore, we could not obtain available informations about electrophysiologic effects of ANP on single human atrial cell, though we observed electrophysiologically reasonable actions of acetylcholine and nicorandil on it.