Karagezian K G, Samvelian V M, Dzhanpoladian E G, Ovsepian L M, Ovakimian S S, Pogosbekova S D, Agababova A A
Cor Vasa. 1975;17(3):212-21.
The authors investigated the cardiotonic effect of monoethanolamine (MEA) and its influence on experimental cardiac hypertrophy in albino rats. In isolated hearts, myocardial cells, and glycerinized fibres as well as in the whole organism of the animals, a distinct cardiotonic effect on MEA was observed, which was most marked in pathological states of the organism. In rats with experimental coarctation of the aorta, MEA dosed 10 mg/kg stimulated, and dosed 60 mg/kg, inhibited the development of myocardial hypertrophy, while the myocardial contractility remained sufficiently preserved. The mechanism of cardiotonic action and the inhibitory effect on the development of myocardial hypertrophy at the dosage of 60 mg/kg are apparently connected with the participation of MEA in tissue metabolic processes contributing to a normalization of tissue respiration, oxidative phosphorylation, and activation of phosphatide-generating reactions, especially to the formation of phospholipids containing ethanolamine, which represent one of the most important membrane formations and components of numerous enzymic systems.
作者研究了单乙醇胺（MEA）的强心作用及其对白化大鼠实验性心肌肥大的影响。在离体心脏、心肌细胞、甘油化纤维以及动物的整个机体中，均观察到MEA有明显的强心作用，在机体的病理状态下最为显著。在实验性主动脉缩窄的大鼠中，剂量为10mg/kg的MEA具有刺激作用，而剂量为60mg/kg时则抑制心肌肥大的发展，同时心肌收缩力仍能充分保持。60mg/kg剂量的MEA的强心作用机制及其对心肌肥大发展的抑制作用显然与MEA参与组织代谢过程有关，这有助于组织呼吸、氧化磷酸化的正常化以及磷脂生成反应的激活，特别是含有乙醇胺的磷脂的形成，而乙醇胺磷脂是最重要的膜结构之一，也是众多酶系统的组成成分。
