【摘要】 心肌细胞Na+ Ca2+交换在缺氧 复氧条件下通过Na+ H+交换、持续性钠电流等途径使胞内Na+升高,进而在去极的静息膜电位、氧自由基共同作用下促进反向的Na+ Ca2+交换,导致胞内Ca2+超载。Ca2+超载引起心肌再灌注损伤、心律失常的发生和细胞高度挛缩甚至死亡。深入研究和探讨缺氧 复氧时Na+ Ca2+交换导致心肌损伤的机理,对于研发临床用于心肌保护的药物有重大意义和广阔前景。更多还原

【Abstract】 During hypoxia-reoxygenation, reverse mode Na⁺-Ca²⁺ exchange results in intracellular Ca²⁺-overload secondary to the raising of intracellular Na⁺, which originates from the increase of Na⁺-H⁺ exchange, persistent sodium current, and the combined action of depolarized membrane potential and hydroxyl radical. The resulting Ca²⁺-overload contributes to reperfusion injury, arrthymogenesis as well as hypercontractureor even death of myocytes. Further investigation into the mechanisms of myocardial injury induced by Na⁺-Ca²⁺ exchange during hypoxia-reoxygenation has great significance and wide prospect in regard to the development of drugs for clinical cardioprotection.更多还原