Pike M M, Kitakaze M, Marban E
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
Am J Physiol. 1990 Dec;259(6 Pt 2):H1767-73. doi: 10.1152/ajpheart.1990.259.6.H1767.
23Na nuclear magnetic resonance (NMR) spectroscopy was utilized to measure intracellular Na+ in perfused ferret hearts exposed to the shift reagent dysprosium triethylenetramine-hexa-acetic acid [Dy(TTHA)3-]. The intracellular Na+ signal was small under normal perfusion conditions; resolution was enhanced by using a Jump-Return NMR pulse protocol. During 20 min of total global ischemia at 30 degrees C, intracellular Na+ concentration ([Na+]i) increased steadily to a peak value fivefold greater than control. [Na+]i declined monotonically back to control levels within 9 min of reperfusion. In contrast, the mean contractile pressure only recovered to 54% of control levels. Thus major alterations in Na+ homeostasis occur during severe ischemia. [Na+] recovers rapidly during reperfusion and is therefore dissociated from the lingering postischemic depression of contractile function known as "stunning."
利用23Na核磁共振（NMR）光谱法测量暴露于位移试剂三乙烯四胺六乙酸镝[Dy(TTHA)3-]的灌注雪貂心脏中的细胞内Na+。在正常灌注条件下，细胞内Na+信号很小；通过使用Jump-Return NMR脉冲方案提高了分辨率。在30℃下完全性全心缺血20分钟期间，细胞内Na+浓度（[Na+]i）稳步增加至比对照高五倍的峰值。[Na+]i在再灌注9分钟内单调下降至对照水平。相比之下，平均收缩压仅恢复至对照水平的54%。因此，在严重缺血期间会发生Na+稳态的主要改变。[Na+]在再灌注期间迅速恢复，因此与称为“顿抑”的缺血后收缩功能持续抑制无关。
