Renaud J F
Centre de Biochimie du CNRS, Faculté des Sciences, Nice, France.
Cardiovasc Drugs Ther. 1988 Mar;1(6):677-86. doi: 10.1007/BF02125756.
The effects of trimetazidine were studied on plasma membrane structures of cardiac cells which control excitability, as well as on cardiac cells that were cultured in normal physiologic conditions and after intracellular acidification. When cardiac cells were kept in normal physiologic conditions, trimetazidine at concentrations ranging from 10(-8) to 3.10(-4) M interacted neither directly nor indirectly with the major ionic transporter systems of cardiac cells, such as ionic channels (Na+, K+), ATPase, Na+/H+, and Na+/Ca2+ exchange systems. Under acid-load conditions trimetazide acts in a dose- and time-dependent manner, in limiting the accumulation of Na+ and Ca2+ inside cardiac cells and depressing intracellular cell acidosis. It is proposed that trimetazidine plays a key role in limiting the intracellular accumulation of protons that is responsible for cell acidosis during ischemia. Trimetazidine, in protecting cardiac cells against accumulation of protons, limits accumulation of Na+ and Ca2+.
研究了曲美他嗪对控制兴奋性的心肌细胞质膜结构的影响，以及对在正常生理条件下培养的心肌细胞和细胞内酸化后的心肌细胞的影响。当心肌细胞处于正常生理条件下时，浓度范围为10（-8）至3.10（-4）M的曲美他嗪与心肌细胞的主要离子转运系统，如离子通道（Na +、K +）、ATP酶、Na + /H +和Na + /Ca2 +交换系统，既无直接相互作用也无间接相互作用。在酸负荷条件下，曲美他嗪以剂量和时间依赖性方式起作用，限制心肌细胞内Na +和Ca2 +的积累，并减轻细胞内酸中毒。有人提出，曲美他嗪在限制缺血期间导致细胞酸中毒的质子在细胞内积累方面起关键作用。曲美他嗪在保护心肌细胞免受质子积累的同时，限制了Na +和Ca2 +的积累。
