心肌Na+-Ca2+ 交换和缺氧-复氧

心肌细胞Na^ -Ca^2 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^ -Ca^2 交换，导致胞内Ca^2 超栽。Ca^2 超栽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^ -Ca^2 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。

Myocardial Na+-Ca2+Exchange and Hypoxia-Reoxygenation

During hypoxia-reoxygenation, reverse mode Na~(+)-Ca~(2+) exchange results in intracellular Ca~(2+)-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 Ca~(2+)-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~(+)-Ca~(2+) exchange during hypoxia-reoxygenation has great significance and wide prospect in regard to the development of drugs for clinical cardioprotection.