首页> 外文期刊>Japanese Journal of Pharmacology >RECOVERING EFFECT OF ACETYLCHOLINE ON THE DEPRESSED ATRIAL TRANSMEMBRANE POTENTIAL OF THE RESERPINIZED RABBIT BY THE ADRENOLYTICS
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RECOVERING EFFECT OF ACETYLCHOLINE ON THE DEPRESSED ATRIAL TRANSMEMBRANE POTENTIAL OF THE RESERPINIZED RABBIT BY THE ADRENOLYTICS

机译:肾上腺素对乙酰胆碱对重组兔抑郁的心房膜电位的恢复作用

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References(26) Cited-By(2) In the previous paper (1) the effects of the adrenolytics on the transmembrane potential of the extirpated rabbit's heart were reported. The adrenolytics exerted depressive effects on the action potential, i.e. decrease in the rate, prolongation of the de- and re- polarization phases and depression of the amplitude with subsequent complete abolition of the atrial non-pacemaker potential. The resting potential was slightly decreased. However, the pacemaker potential, though it was slightly or moderately depressed, continued to fire rhythmically. In this condition addition of adrenaline or noradrenaline in the concentration which exerted a positive inotropic effect on the intact heart restarted the potential rhythm. However, the recovery of the transmembrane potential was transient and incomplete even by addition of higher concentration of either amine. Physiological role of noradrenaline in the heart (2-5) on the spontaneous automaticity of the atrium has not been hitherto fully elucidated. Though the effects of the adrenolytics on the transmembrane potential of the heart may relate with the adrenergic mechanism, Matsuo et al. (6) have shown the increase of noradrenaline in the rabbit's heart in response to the intravenous injection of dibenamine (10 mg/kg) but not to the same procedure of yohimbine (5 mg/kg) or chlorpromazine (5 mg/kg). The biphasic responses of the heart to acetylcholine have been observed by several authors (7-14). The restarting effect of acetylcholine on the atrial preparation in which rhythmical contraction had been abolished by quinidine, eserine and paludrine (12, 13) and by the lowering of environmental temperature (14) has been reported. The present investigation has been attempted to elucidate the mechanism of the standstill of the atrial transmembrane potential induced by the adrenolytics by studying the restarting and recovering effects of adrenaline, noradrenaline and acetylcholine in the isolated atrium of rabbit which had been pretreated with reserpine. It has been also expected to explain the mode of action of the endogenous catecholamine and acetylcholine on the atrial non-pacemaker potential.
机译:参考文献(26)Cited-By(2)在先前的文章中(1)报道了肾上腺皮质激素对脱兔兔子心脏跨膜电位的影响。肾上腺皮质激素对动作电位产生抑制作用,即速率降低,去极化和复极化阶段的延长以及振幅的降低,随后完全消除了心房非起搏器的电位。静息电位略有下降。然而,起搏器的潜力尽管被轻度或中度压抑,但仍在有节奏地激发。在这种情况下,以对完好的心脏产生正性肌力作用的浓度添加肾上腺素或去甲肾上腺素重新开始潜在的节律。然而,即使通过添加更高浓度的任一胺,跨膜电位的恢复也是短暂且不完全的。迄今为止,尚未充分阐明去甲肾上腺素在心脏中的生理作用(2-5)对自发性心房的作用。尽管肾上腺皮质激素对心脏跨膜电位的影响可能与肾上腺素能机制有关,Matsuo等人。 (6)已显示,对静脉注射苯二胺(10 mg / kg)而不是对育亨宾(5 mg / kg)或氯丙嗪(5 mg / kg)的相同操作,兔子心脏中的去甲肾上腺素增加。几位作者已经观察到心脏对乙酰胆碱的双相反应(7-14)。据报道,乙酰胆碱对心房颤动的起效作用,其中奎尼丁,色氨酸和paludrine(12,13)和环境温度的降低(14)消除了节律性收缩。本研究试图通过研究肾上腺素,去甲肾上腺素和乙酰胆碱在经利血平预处理的家兔离体心房中的重启和恢复作用,阐明由肾上腺皮质激素引起的心房跨膜电位停滞的机制。还已经预期可以解释内源性儿茶酚胺和乙酰胆碱对心房非起搏器电位的作用方式。

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