Intracellular sodium flux and high-energy phosphorus metabolites in ischemic skeletal muscle.
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.
Department of Surgery, Hospital of the University of Pennsylvania, Philadelphia.
H
H
Blum
M D
MD
Schnall
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B
Chance
G P
GP
Buzby
D000227:Adenine Nucleotides / Q000378:metabolism*; D000818:Animals; D007511:Ischemia / Q000378:metabolism*; D007700:Kinetics; D009682:Magnetic Resonance Spectroscopy / Q000379:methods; D008297:Male; D009132:Muscles / Q000098:blood supply* / Q000378:metabolism; D009243:NAD / Q000378:metabolism*; D010710:Phosphates / Q000378:metabolism*; D010725:Phosphocreatine / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D012016:Reference Values; D012964:Sodium / Q000378:metabolism*; D013816:Thermodynamics
D000227:Adenine Nucleotides; D010710:Phosphates; D010725:Phosphocreatine; D009243:NAD; D012964:Sodium