Pike M M, Luo C S, Clark M D, Kirk K A, Kitakaze M, Madden M C, Cragoe E J, Pohost G M
Department of Medicine, University of Alabama at Birmingham 35294.
Am J Physiol. 1993 Dec;265(6 Pt 2):H2017-26. doi: 10.1152/ajpheart.1993.265.6.H2017.
Interleaved 23Na- and 31P-nuclear magnetic resonance (NMR) spectra were continuously collected on perfused rat hearts subjected to low-flow ischemia (30 min, 10% flow) or zero-flow ischemia (21 min) followed by reperfusion. During untreated low-flow and zero-flow ischemia, intracellular Na+ (Nai+) increased by 53 +/- 11 (+/- SE) and 78 +/- 8%, respectively, and remained elevated for zero-flow hearts. However, during both low- and zero-flow ischemia, Nai+ did not increase in hearts treated with the Na(+)-H+ exchange inhibitor, 5-(N-ethyl-N-isopropyl)amiloride (EIPA). The pH decreases during ischemia were unchanged. EIPA treatment reduced ATP depletion during ischemia. During reperfusion from zero-flow ischemia, EIPA-treated hearts displayed more rapid and extensive recoveries of phosphocreatine and ATP. Recovery of left ventricular developed pressure was improved for zero-flow hearts treated with EIPA during the ischemic period exclusively (104 +/- 13%) compared with untreated hearts (36 +/- 21%). These data indicate that Na(+)-H+ exchange is an important mechanism for Nai+ accumulation, but not for pH regulation, during myocardial ischemia. Additionally, Nai+ homeostasis plays an important role in the postischemic recovery of cellular energy and ventricular function.
对经历低流量缺血（30分钟，10%流量）或零流量缺血（21分钟）然后再灌注的灌注大鼠心脏连续收集交错的23Na和31P核磁共振（NMR）光谱。在未经处理的低流量和零流量缺血期间，细胞内Na+（Nai+）分别增加了53±11（±SE）和78±8%，并且在零流量心脏中仍保持升高。然而，在低流量和零流量缺血期间，用Na(+)-H+交换抑制剂5-（N-乙基-N-异丙基）氨氯吡脒（EIPA）处理的心脏中Nai+并未增加。缺血期间的pH降低没有变化。EIPA处理减少了缺血期间的ATP消耗。在从零流量缺血再灌注期间，EIPA处理的心脏显示磷酸肌酸和ATP的恢复更快且更广泛。仅在缺血期用EIPA处理的零流量心脏的左心室舒张末压恢复（104±13%）比未处理的心脏（36±21%）有所改善。这些数据表明，在心肌缺血期间，Na(+)-H+交换是Nai+积累的重要机制，但不是pH调节的重要机制。此外，Nai+稳态在缺血后细胞能量和心室功能的恢复中起重要作用。
