Kawarabayashi T, Kishikawa T, Sugimori H
Am J Obstet Gynecol. 1986 Sep;155(3):671-6. doi: 10.1016/0002-9378(86)90305-4.
Spontaneous intracellular electrical activity and contraction of pregnant human myometrium were recorded by the single sucrose-gap method, and the effects of oxytocin on the muscle were studied. In pregnant human myometrium at term, both plateau and spike types of action potentials were observed. All contractions were well synchronized with each action potential. Oxytocin, 10(-2) U/ml, potentiated spontaneous contractions by enhancing the plateau part of action potentials; spike-type configuration became plateau. When extracellular ionized calcium was removed, spontaneous activities disappeared, while 10(-2) U/ml of oxytocin could evoke action potentials and contractions but these were smaller than those of the controls. Spontaneous activities also disappeared when ionized calcium was increased to 5 mmol/L, but oxytocin evoked plateau potentials and contractions remarkably. Diltiazem (ionized calcium antagonist), 10(-6) gm/ml, suppressed the spontaneous activity, but oxytocin evoked action potentials and contractions in high frequency, the duration of the action potential being short and the contraction being small. In the presence of 10(-4) gm/ml of diltiazem, 10(-2) U/ml of oxytocin could not evoke any action potentials but did evoke small and long contractures, while in a high ionized potassium contracture experiment, oxytocin potentiated the tonic phase. These results suggest that oxytocin can increase spontaneous contractions by enhancing plateau potentials and that this effect requires sufficient extracellular ionized calcium. In this potentiation, the effects on frequency and amplitude of contractions might vary. It is also suggested that oxytocin may evoke a contracture in the absence of an action potential by releasing calcium from intracellular storage sites.
采用单蔗糖间隙法记录了妊娠晚期人子宫肌层的自发细胞内电活动和收缩情况,并研究了催产素对该肌肉的作用。在足月妊娠的人子宫肌层中,观察到了平台型和锋电位型两种动作电位。所有收缩均与每个动作电位良好同步。10(-2)U/ml的催产素通过增强动作电位的平台部分来增强自发收缩;锋电位型构型变为平台型。去除细胞外游离钙后,自发活动消失,而10(-2)U/ml的催产素仍可诱发动作电位和收缩,但这些比对照组的小。当游离钙增加到5mmol/L时,自发活动也消失,但催产素能显著诱发平台电位和收缩。10(-6)g/ml的地尔硫䓬(一种游离钙拮抗剂)可抑制自发活动,但催产素能高频诱发动作电位和收缩,动作电位持续时间短,收缩幅度小。在存在10(-4)g/ml地尔硫䓬的情况下,10(-2)U/ml的催产素不能诱发任何动作电位,但能诱发小而持久的挛缩,而在高钾挛缩实验中,催产素增强了强直期。这些结果表明,催产素可通过增强平台电位来增加自发收缩,且这种作用需要足够的细胞外游离钙。在这种增强作用中,对收缩频率和幅度的影响可能有所不同。还表明,催产素可能通过从细胞内储存部位释放钙而在无动作电位的情况下诱发挛缩。