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Metabolic and ionic changes in muscle during hemorrhagic shock.
H Blum1, M D Schnall, P F Renshaw
1Department of Surgery, Hospital of the University of Pennsylvania, Philadelphia.
Circulatory Shock
|December 1, 1988
Summary
Intracellular sodium (Nai) levels in rat muscle remained stable during shock until the phosphorylation ratio fell significantly. This indicates a critical threshold for Nai increase and potential Na+-K+ antiport dysfunction.
Area of Science:
- Physiology
- Biochemistry
- NMR Spectroscopy
Background:
- Understanding cellular ion balance is crucial for diagnosing shock.
- Noninvasive techniques are needed to monitor cellular changes during shock.
Purpose of the Study:
- To investigate the behavior of intracellular sodium (Nai) and phosphorus metabolites during hemorrhagic shock in rat leg muscle.
- To determine the relationship between the phosphorylation ratio and Nai increase during shock.
Main Methods:
- Concurrent noninvasive 31P and 23Na NMR spectroscopy was used.
- A paramagnetic shift reagent, dysprosium triethylenetetramine hexaacetic acid, was employed.
- Male Wistar rats were subjected to controlled hypotension (40 mm Hg mean arterial blood pressure).
Main Results:
- Intracellular sodium (Nai) did not increase until decompensatory shock.
- Adenosine triphosphate (ATP) levels remained stable until decompensation, while phosphocreatine decreased.
- Nai increase began when the phosphorylation ratio (PR) fell below log(PR) = 3.21 +/- .42, at a rate of 7.97 +/- 0.60 meq/l/hr.
- This Nai increase correlated with a two-fold rise in Na+ permeability.
Conclusions:
- A critical threshold in the phosphorylation ratio precedes significant intracellular sodium accumulation during shock.
- The observed Nai increase is energetically consistent with the function of the Na+-K+ antiport.
- NMR spectroscopy provides valuable insights into cellular metabolic and ionic changes during shock.