Metabolic and ionic changes in muscle during hemorrhagic shock.
We have employed concurrent noninvasive 31P and 23Na NMR spectroscopy in conjunction with the paramagnetic shift reagent dysprosium triethylenetetramine hexaacetic acid to observe the intracellular sodium and phosphorus signals in rat leg muscle. Male Wistar rats were bled to a mean arterial blood pressure of 40 mm Hg and were maintained at that pressure. Until decompensatory shock was reached, no increase in intracellular sodium (Nai) was found. Although the high energy storage metabolite phosphocreatine fell with time during shock, ATP did not decrease until decompensation. When the phosphorylation ratio, PR = [ATP]/[ADP][Pi], fell below log(PR) = 3.21 +/- .42, Nai increase commenced at a rate of 7.97 +/- 0.60 meq/l/hr. This corresponds to a two-fold increase in Na permeability compared to normal muscle. A calculation of the free energy available from hydrolysis of ATP at the above value of PR yields -11.7 kcal/mol which is essentially equal to the value of 11.8 kcal/mol which we calculate is needed to run the Na+-K+ antiport through one cycle under normal physiologic conditions.
Blum
H
H
Department of Surgery, Hospital of the University of Pennsylvania, Philadelphia.
Schnall
M D
MD
Renshaw
P F
PF
Buzby
G P
GP
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D004734:Energy Metabolism; D006863:Hydrogen-Ion Concentration; D007700:Kinetics; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D009132:Muscles / Q000378:metabolism*; D010725:Phosphocreatine / Q000378:metabolism; D010758:Phosphorus / Q000378:metabolism; D010766:Phosphorylation; D051381:Rats; D011919:Rats, Inbred Strains; D012771:Shock, Hemorrhagic / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism
D010725:Phosphocreatine; D010758:Phosphorus; D000255:Adenosine Triphosphate; D012964:Sodium