Hisatome I, Arita M
Department of Physiology, Oita Medical University, Hasama, Japan.
Cardiovasc Res. 1995 Jan;29(1):65-73.
The aim was to study the effects of catecholamines (isoprenaline and noradrenaline) on the action potential upstroke and conduction velocity in guinea pig ventricular papillary muscles.
The upstroke velocity and the conduction velocity of the action potential were recorded by conventional two-microelectrode techniques in the guinea pig ventricular papillary muscle superfused with normoxic and hypoxic Tyrode solution of various potassium concentrations ([K+]o 2.7-16.7 mM), stimulated at 0.2 Hz.
Under normoxic conditions, the upstroke of action potentials is composed of two components, dV/dtmax,fast followed by dV/dtmax,slow, when the muscle were perfused with relatively high [K+]o (10.8-16.7 mM). The dV/dtmax,fast is a measure of the residual (mostly inactivated) sodium current, while the dV/dtmax,slow is a measure of calcium current. The conduction velocity at 13-17 mM [K+]o ranged from 30-40 cm.s-1 (slow conduction) with depolarised membrane potentials of about -60 mV. Isoprenaline in increasing concentrations (0.01-1 microM) did not significantly alter the conduction velocity but altered the ionic channels responsible for the slow conduction from residual sodium channel to calcium channel. In the presence of D600 (2 microM) or 1-verapamil (2.2 microM), isoprenaline (0.1 microM) rapidly decreased dV/dtmax,fast without increasing dV/dtmax,slow and a conduction block occurred. In the presence of pindolol (2 microM), all the effects of isoprenaline on dV/dtmax,fast, dV/dtmax,slow, and conduction velocity were abolished. Noradrenaline has the same effects as isoprenaline, although the potency was much less. Under hypoxic conditions, the effects of catecholamines on the dV/dtmax,fast was the same as under normoxic conditions.
Catecholamines alter the ionic channel responsible for the slow conduction of reentry circuit from residual sodium to calcium channel, or vice versa, depending on the local concentrations of catecholamines. In the presence of a calcium antagonist, catecholamines strongly depress the (dV/dtmax,fast dependent) slow conduction, leading to a complete block of conduction, under both normoxia and hypoxia.
研究儿茶酚胺（异丙肾上腺素和去甲肾上腺素）对豚鼠心室乳头肌动作电位上升支及传导速度的影响。
采用传统双微电极技术，在灌流不同钾浓度（[K⁺]ₒ 2.7 - 16.7 mM）的常氧和低氧台氏液的豚鼠心室乳头肌中，以0.2 Hz频率刺激，记录动作电位的上升速度和传导速度。
在常氧条件下，当肌肉用相对高的[K⁺]ₒ（10.8 - 16.7 mM）灌流时，动作电位的上升支由两个成分组成，即快速的dV/dtmax,fast，随后是缓慢的dV/dtmax,slow。dV/dtmax,fast是残余（大多失活）钠电流的指标，而dV/dtmax,slow是钙电流的指标。在13 - 17 mM [K⁺]ₒ时，传导速度范围为30 - 40 cm·s⁻¹（慢传导），膜电位去极化至约 -60 mV。浓度递增的异丙肾上腺素（0.01 - 1 μM）未显著改变传导速度，但改变了负责慢传导的离子通道，从残余钠通道转变为钙通道。在存在D600（2 μM）或维拉帕米（2.2 μM）时，异丙肾上腺素（0.1 μM）迅速降低dV/dtmax,fast而不增加dV/dtmax,slow，并发生传导阻滞。在存在吲哚洛尔（2 μM）时，异丙肾上腺素对dV/dtmax,fast、dV/dtmax,slow和传导速度的所有作用均被消除。去甲肾上腺素具有与异丙肾上腺素相同 的作用，尽管效力要低得多。在低氧条件下，儿茶酚胺对dV/dtmax,fast的作用与常氧条件下相同。
儿茶酚胺根据其局部浓度改变负责折返环慢传导的离子通道，从残余钠通道转变为钙通道，反之亦然。在存在钙拮抗剂的情况下，儿茶酚胺在常氧和低氧条件下均强烈抑制（依赖dV/dtmax,fast的）慢传导，导致完全性传导阻滞。
