31P and 23Na NMR spectroscopy of normal and ischemic rat skeletal muscle. Use of a shift reagent in vivo.

J. A. Balschi, J. A. Bittl, Charles Jr Springer, J. S. Ingwall

Research output: Contribution to journalArticle

33 Citations (Scopus)

Abstract

23Na NMR spectroscopy was used 1, to define the distribution of the shift reagent for cations, triethylenetetraminehexaacetatedysprosium(III), DyTTHA3-, in the living rat; 2, to define the characteristics of the Na resonances reporting intra- and extracellular Na+ in skeletal muscle in vivo; and 3, to calculate the Na+ concentrations in the intra- and extracellular spaces of the gastrocnemius muscle during well-perfused and ischemic conditions. The concentration of DyTTHA3- infused intravenously into the jugular vein of the living rat reached a maximum value of 8-9 mM in the extracellular space of the muscle after ca 40 min of infusion. This allowed excellent discrimination of extra- and intracellular Na signals (Nao and Nai, respectively) and did not spoil the resolution of concurrent 31P NMR spectra. Infusion of shift reagent changed neither hemodynamic performance of the rat nor the high-energy phosphate content of skeletal muscle. Shift reagent enters ca 15% (v/w) of the rat body weight; this corresponds to almost all of the "fast" or rapidly permeable extracellular space. It is excreted from the body with a pseudo-first order rate constant of 0.0158 min-1. In resting muscle, we estimate that [Na+]i is 3-5 mM and, in muscle perfused with the sodium salt of the shift reagent, that [Na+]o in the fast exchangeable extracellular space is 166 mM. During 11 h of ischemia at 37 degrees C, the area of the Nai+ signal area monotonically increased sixfold. Based on estimates for maximum changes in fluid shifts reported by the decrease in the area of the Nao signal area, we calculate that the lower limit for [Na+]i after 11 h of ischemia is 27 mM. The NMR-visibility factors for the extracellular and intracellular Na+ signals are essentially the same. This study demonstrates that the shift reagent DyTTHA3- is acutely non-toxic and that the 23Na NMR spectra obtained can be used to quantitate [Na+]o and [Na+]i in tissues in vivo. Using this technique, we found that the transmembrane sodium gradient fell from ca 35 in well-perfused skeletal muscle to less than 6 during prolonged ischemia.

Original languageEnglish (US)
Pages (from-to)47-58
Number of pages12
JournalNMR in Biomedicine
Volume3
Issue number2
StatePublished - Apr 1990
Externally publishedYes

Fingerprint

Nuclear magnetic resonance spectroscopy
Muscle
Extracellular Space
Rats
Skeletal Muscle
Magnetic Resonance Spectroscopy
Ischemia
Muscles
Nuclear magnetic resonance
Sodium
Fluid Shifts
Intracellular Space
Jugular Veins
Cations
Hemodynamics
Salts
Phosphates
Body Weight
Visibility
Rate constants

ASJC Scopus subject areas

  • Biophysics

Cite this

31P and 23Na NMR spectroscopy of normal and ischemic rat skeletal muscle. Use of a shift reagent in vivo. / Balschi, J. A.; Bittl, J. A.; Springer, Charles Jr; Ingwall, J. S.

In: NMR in Biomedicine, Vol. 3, No. 2, 04.1990, p. 47-58.

Research output: Contribution to journalArticle

@article{863f5b6c1c0a4307a11cf3299e08e016,
title = "31P and 23Na NMR spectroscopy of normal and ischemic rat skeletal muscle. Use of a shift reagent in vivo.",
abstract = "23Na NMR spectroscopy was used 1, to define the distribution of the shift reagent for cations, triethylenetetraminehexaacetatedysprosium(III), DyTTHA3-, in the living rat; 2, to define the characteristics of the Na resonances reporting intra- and extracellular Na+ in skeletal muscle in vivo; and 3, to calculate the Na+ concentrations in the intra- and extracellular spaces of the gastrocnemius muscle during well-perfused and ischemic conditions. The concentration of DyTTHA3- infused intravenously into the jugular vein of the living rat reached a maximum value of 8-9 mM in the extracellular space of the muscle after ca 40 min of infusion. This allowed excellent discrimination of extra- and intracellular Na signals (Nao and Nai, respectively) and did not spoil the resolution of concurrent 31P NMR spectra. Infusion of shift reagent changed neither hemodynamic performance of the rat nor the high-energy phosphate content of skeletal muscle. Shift reagent enters ca 15{\%} (v/w) of the rat body weight; this corresponds to almost all of the {"}fast{"} or rapidly permeable extracellular space. It is excreted from the body with a pseudo-first order rate constant of 0.0158 min-1. In resting muscle, we estimate that [Na+]i is 3-5 mM and, in muscle perfused with the sodium salt of the shift reagent, that [Na+]o in the fast exchangeable extracellular space is 166 mM. During 11 h of ischemia at 37 degrees C, the area of the Nai+ signal area monotonically increased sixfold. Based on estimates for maximum changes in fluid shifts reported by the decrease in the area of the Nao signal area, we calculate that the lower limit for [Na+]i after 11 h of ischemia is 27 mM. The NMR-visibility factors for the extracellular and intracellular Na+ signals are essentially the same. This study demonstrates that the shift reagent DyTTHA3- is acutely non-toxic and that the 23Na NMR spectra obtained can be used to quantitate [Na+]o and [Na+]i in tissues in vivo. Using this technique, we found that the transmembrane sodium gradient fell from ca 35 in well-perfused skeletal muscle to less than 6 during prolonged ischemia.",
author = "Balschi, {J. A.} and Bittl, {J. A.} and Springer, {Charles Jr} and Ingwall, {J. S.}",
year = "1990",
month = "4",
language = "English (US)",
volume = "3",
pages = "47--58",
journal = "NMR in Biomedicine",
issn = "0952-3480",
publisher = "John Wiley and Sons Ltd",
number = "2",

}

TY - JOUR

T1 - 31P and 23Na NMR spectroscopy of normal and ischemic rat skeletal muscle. Use of a shift reagent in vivo.

AU - Balschi, J. A.

AU - Bittl, J. A.

AU - Springer, Charles Jr

AU - Ingwall, J. S.

PY - 1990/4

Y1 - 1990/4

N2 - 23Na NMR spectroscopy was used 1, to define the distribution of the shift reagent for cations, triethylenetetraminehexaacetatedysprosium(III), DyTTHA3-, in the living rat; 2, to define the characteristics of the Na resonances reporting intra- and extracellular Na+ in skeletal muscle in vivo; and 3, to calculate the Na+ concentrations in the intra- and extracellular spaces of the gastrocnemius muscle during well-perfused and ischemic conditions. The concentration of DyTTHA3- infused intravenously into the jugular vein of the living rat reached a maximum value of 8-9 mM in the extracellular space of the muscle after ca 40 min of infusion. This allowed excellent discrimination of extra- and intracellular Na signals (Nao and Nai, respectively) and did not spoil the resolution of concurrent 31P NMR spectra. Infusion of shift reagent changed neither hemodynamic performance of the rat nor the high-energy phosphate content of skeletal muscle. Shift reagent enters ca 15% (v/w) of the rat body weight; this corresponds to almost all of the "fast" or rapidly permeable extracellular space. It is excreted from the body with a pseudo-first order rate constant of 0.0158 min-1. In resting muscle, we estimate that [Na+]i is 3-5 mM and, in muscle perfused with the sodium salt of the shift reagent, that [Na+]o in the fast exchangeable extracellular space is 166 mM. During 11 h of ischemia at 37 degrees C, the area of the Nai+ signal area monotonically increased sixfold. Based on estimates for maximum changes in fluid shifts reported by the decrease in the area of the Nao signal area, we calculate that the lower limit for [Na+]i after 11 h of ischemia is 27 mM. The NMR-visibility factors for the extracellular and intracellular Na+ signals are essentially the same. This study demonstrates that the shift reagent DyTTHA3- is acutely non-toxic and that the 23Na NMR spectra obtained can be used to quantitate [Na+]o and [Na+]i in tissues in vivo. Using this technique, we found that the transmembrane sodium gradient fell from ca 35 in well-perfused skeletal muscle to less than 6 during prolonged ischemia.

AB - 23Na NMR spectroscopy was used 1, to define the distribution of the shift reagent for cations, triethylenetetraminehexaacetatedysprosium(III), DyTTHA3-, in the living rat; 2, to define the characteristics of the Na resonances reporting intra- and extracellular Na+ in skeletal muscle in vivo; and 3, to calculate the Na+ concentrations in the intra- and extracellular spaces of the gastrocnemius muscle during well-perfused and ischemic conditions. The concentration of DyTTHA3- infused intravenously into the jugular vein of the living rat reached a maximum value of 8-9 mM in the extracellular space of the muscle after ca 40 min of infusion. This allowed excellent discrimination of extra- and intracellular Na signals (Nao and Nai, respectively) and did not spoil the resolution of concurrent 31P NMR spectra. Infusion of shift reagent changed neither hemodynamic performance of the rat nor the high-energy phosphate content of skeletal muscle. Shift reagent enters ca 15% (v/w) of the rat body weight; this corresponds to almost all of the "fast" or rapidly permeable extracellular space. It is excreted from the body with a pseudo-first order rate constant of 0.0158 min-1. In resting muscle, we estimate that [Na+]i is 3-5 mM and, in muscle perfused with the sodium salt of the shift reagent, that [Na+]o in the fast exchangeable extracellular space is 166 mM. During 11 h of ischemia at 37 degrees C, the area of the Nai+ signal area monotonically increased sixfold. Based on estimates for maximum changes in fluid shifts reported by the decrease in the area of the Nao signal area, we calculate that the lower limit for [Na+]i after 11 h of ischemia is 27 mM. The NMR-visibility factors for the extracellular and intracellular Na+ signals are essentially the same. This study demonstrates that the shift reagent DyTTHA3- is acutely non-toxic and that the 23Na NMR spectra obtained can be used to quantitate [Na+]o and [Na+]i in tissues in vivo. Using this technique, we found that the transmembrane sodium gradient fell from ca 35 in well-perfused skeletal muscle to less than 6 during prolonged ischemia.

UR - http://www.scopus.com/inward/record.url?scp=0025408609&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0025408609&partnerID=8YFLogxK

M3 - Article

VL - 3

SP - 47

EP - 58

JO - NMR in Biomedicine

JF - NMR in Biomedicine

SN - 0952-3480

IS - 2

ER -