Kardiologiia. 2013;53(4):49-54.
Glutathione is the main redox buffer in cardiomyocytes. The action of ethylglutathione possessing antioxidant properties on functional disorders evoked by 30-minute hypoxia of the isolated rat heart with subsequent reoxygenation has been studied. In control experiments, the presence of glucose (11 mM) in hypoxic perfusate was associated with lesser hypoxic contracture of the myocardium but also with the development of arrhythmias in all experiments, including ventricular tachycardias and fibrillation that may be due to arisen myocardial heterogeneity. After reoxygenation, a half of hearts in this group demonstrated inability to reproduce high rate of stimulation. These alterations were almost completely prevented when ethylglutathione (0.2 mM) was added into hypoxic perfusate. Its presence in the solution also facilitated 1.5-fold improvement of cardiac function recovery after reoxygenation. The results suggest that the protective action of ethylglutathione may be due to a reduced oxidative modification of ionic transport proteins. At non-glucose hypoxic perfusion, myocardial contracture was higher but abovementioned functional disorders did not arise, and ethylglutathione addition was inefficient.
谷胱甘肽是心肌细胞中的主要氧化还原缓冲剂。研究了具有抗氧化特性的乙基谷胱甘肽对离体大鼠心脏30分钟缺氧及随后复氧所诱发的功能紊乱的作用。在对照实验中，缺氧灌注液中葡萄糖（11 mM）的存在与心肌较小的缺氧挛缩有关，但在所有实验中也与心律失常的发生有关，包括室性心动过速和颤动，这可能是由于心肌异质性的出现。复氧后，该组一半的心脏表现出无法恢复高频率刺激。当向缺氧灌注液中加入乙基谷胱甘肽（0.2 mM）时，这些改变几乎完全得到预防。溶液中乙基谷胱甘肽的存在还使复氧后心脏功能恢复提高了1.5倍。结果表明，乙基谷胱甘肽的保护作用可能是由于离子转运蛋白的氧化修饰减少。在无葡萄糖的缺氧灌注时，心肌挛缩较高，但未出现上述功能紊乱，添加乙基谷胱甘肽无效。
