Elfellah M S, Khan M T
Arch Int Pharmacodyn Ther. 1986 Aug;282(2):288-97.
In the rat Langendorff heart perfused with Krebs solution and prelabeled with [3H]-noradrenaline, ouabain caused arrhythmia as well as significant inhibition of spontaneous and electrically stimulated release of tritium. However, there is no causal relationship between the inhibition of tritium release and the occurrence of arrhythmia. Chromatographic analysis of the labeled perfusate suggests that ouabain reduced intact [3H]-noradrenaline fraction obtained during electrical stimulation. The inhibitory effect of ouabain on electrically stimulated release was completely antagonized by atropine, but not by indomethacin and phenoxybenzamine. However, none of the above agents antagonized the inhibitory effect of ouabain on spontaneous tritium release. Infusion of acetylcholine also inhibited electrically stimulated tritium release, and this effect was largely abolished by atropine. Thus it appears that in high concentrations, ouabain may release acetylcholine, which in turn activates presynaptic muscarinic inhibitory receptors leading to inhibition of noradrenaline release from the rat heart.
在用Krebs溶液灌注并用[3H]-去甲肾上腺素预标记的大鼠Langendorff心脏中，哇巴因可引起心律失常，并显著抑制氚的自发释放和电刺激释放。然而，氚释放的抑制与心律失常的发生之间没有因果关系。对标记灌注液的色谱分析表明，哇巴因降低了电刺激期间获得的完整[3H]-去甲肾上腺素部分。哇巴因对电刺激释放的抑制作用完全被阿托品拮抗，但消炎痛和酚苄明不能拮抗。然而，上述药物均不能拮抗哇巴因对自发氚释放的抑制作用。乙酰胆碱的输注也抑制了电刺激的氚释放，这种作用在很大程度上被阿托品消除。因此，似乎在高浓度下，哇巴因可能释放乙酰胆碱，而乙酰胆碱又激活突触前毒蕈碱抑制受体，导致大鼠心脏去甲肾上腺素释放受到抑制。
