Intracellular sodium flux and high-energy phosphorus metabolites in ischemic skeletal muscle.
Intracellular sodium flux and high-energy phosphorus metabolites in ischemic skeletal muscle.
复制标题
缺血骨骼肌中的细胞内钠通量和高能磷代谢物。
DOI：
10.1152/ajpcell.1988.255.3.c377
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Buzby,GP
中科院分区：
文献类型：
--
作者：
Blum,H;Schnall,MD;Chance,B;Buzby,GP
我们用同时的~(31)P和~(23)Na核磁共振波谱，结合顺磁移位试剂三聚磷酸和三乙烯四胺六乙酸，观察了大鼠腿肌细胞内钠和磷的信号。在诱发腿部缺血的情况下，我们发现磷酸化电位缓慢下降。在一个临界值，伴随着Na+-K+反向转运体的能量失效，细胞内的钠信号开始增加。其临界值为：对数为3.12+/-0.32；pH为6.86+/-0.13；Na+内流分别为5.1+/-4.3和4.0+/-1.3mol.l-1.h-1。
We have employed concurrent 31P- and 23Na-nuclear magnetic resonance (NMR) spectroscopy in conjunction with the paramagnetic shift reagents dysprosium-chelated tripolyphosphate and triethylenetetramine-hexa-acetic acid to observe the intracellular sodium and phosphorus signals in rat leg muscle. With induced ischemia in the leg, we find slowly falling phosphorylation potential. At a critical value of, associated with energetic failure of the Na+-K+ antiport, the intracellular sodium signal begins to increase. We find the following critical values: log, 3.12 +/- 0.32; pH, 6.86 +/- 0.13; Na+ influx with and without ouabain, 5.1 +/- 4.3 and 4.0 +/- 1.3 mol.l-1.h-1, respectively.