NMR MEASUREMENTS OF NA+ AND CELLULAR-ENERGY IN ISCHEMIC RAT-HEART - ROLE OF NA+-H+ EXCHANGE
NMR MEASUREMENTS OF NA+ AND CELLULAR-ENERGY IN ISCHEMIC RAT-HEART - ROLE OF NA+-H+ EXCHANGE
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DOI：
10.1152/ajpheart.1993.265.6.h2017
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发表时间：
1993-12-01
影响因子：
--
通讯作者：
POHOST, GM
中科院分区：
文献类型：
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作者：
PIKE, MM;LUO, CS;POHOST, GM
连续采集灌注大鼠心脏低流量缺血（30 min， 10%流量）或零流量缺血（21 min）后再灌注时的Na-23和p -31交错核磁共振（NMR）谱。在未处理的低流量和零流量缺血期间，细胞内Na+ (Na(i)+)分别增加53 +/- 11 （+/- SE）和78 +/- 8%，并且在零流量心脏中保持升高。然而，在低流量和零流量缺血期间，使用Na+- h +交换抑制剂5-（n -乙基- n -异丙基）酰胺（EIPA）处理的心脏Na(i)+没有增加。缺血时pH值的下降没有变化。EIPA治疗减少了缺血时ATP的消耗。在零流缺血再灌注期间，经eipa处理的心脏显示出更快速和广泛的磷酸肌酸和ATP恢复。与未治疗的心脏（36 +/- 21%）相比，EIPA治疗的零流量心脏在缺血期间左室发展压力的恢复（104 +/- 13%）得到改善。这些数据表明，在心肌缺血时，Na+-H+交换是Na(i)+积累的重要机制，而不是pH调节机制。此外，Na+稳态在缺血后细胞能量和心室功能的恢复中起着重要作用。
Interleaved Na-23- and P-31-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+ (Na(i)+) increased by 53 +/- 11 (+/- SE) and 78 +/- 8%, respectively, and remained elevated for zero-flow hearts. However, during both low- and zero-flow ischemia, Na(i)+ 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 Na(i)+ accumulation, but not for pH regulation, during myocardial ischemia. Additionally, Na+ homeostasis plays an important role in the postischemic recovery of cellular energy and ventricular function.