Effects of ischemia on intracellular sodium and phosphates in the in vivo rat liver

Zhao Fan Xia, Jureta W. Horton, Pi Yu Zhao, Evelyn E. Babcock, A. Dean Sherry, Craig R. Malloy

Research output: Contribution to journalArticle

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Abstract

Metabolic factors that influence the transition from reversible to irreversible ischemic injury were studied in the rat liver in vivo with 31P-nuclear magnetic resonance (NMR) spectroscopy. Hepatic ischemia for 15, 35, or 65 min was produced by occlusion of the hepatic artery and portal vein in rats. Ischemia caused a rapid decrease in the ATP concentration ([ATP])- to-P(i) concentration ratio and pH within 5 min, but there was little change in these variables detectable by 31P-NMR with longer periods of ischemia. After reperfusion, the [ATP] and P(i) concentration returned toward normal values in livers exposed to 15 or 35 min of ischemia, but 65 min of ischemia were associated with only modest recovery in [ATP], and the [ATP] later decreased. Because the 31P-NMR spectrum was similar after brief compared with prolonged ischemia, it appears that neither ATP depletion, P(i) accumulation, nor acidosis predicts metabolic recovery. Hepatic intracellular Na+ was also measured in separate groups of animals by 23Na-NMR in the presence of a shift agent, thulium (III) 1,4,7,10-tetraazacyclododecane- 1,4,7,10-tetrakis(methylene-phosphonate) (TmDOTP5-), and by atomic absorption spectroscopy. Under baseline conditions, the concentration of intracellular Na+ was 15.2 mM by atomic absorption spectroscopy and 16.5 mM by 23Na-NMR. Although the 31P-NMR spectrum responded very rapidly to the onset of ischemia, intracellular Na+ concentration measured by 23Na-NMR increased gradually but steadily at ~1.0 mM/min during early (up to 15 min) ischemia. These observations demonstrate that a rise in intracellular Na+ does occur during early ischemia, that TmDOTP5- can be applied in vivo for analysis of intracellular Na+ in the ischemic liver, and that 31P-NMR spectroscopy is very sensitive to early ischemic injury.

Original languageEnglish (US)
Pages (from-to)1395-1403
Number of pages9
JournalJournal of Applied Physiology
Volume81
Issue number3
StatePublished - Sep 1996

Fingerprint

Ischemia
Magnetic Resonance Spectroscopy
Liver
Adenosine Triphosphate
Spectrum Analysis
Thulium
sodium phosphate
Organophosphonates
Hepatic Veins
Hepatic Artery
Wounds and Injuries
Portal Vein
Acidosis
Reperfusion
Reference Values

Keywords

  • adenosine triphosphate
  • atomic absorption spectroscopy
  • bioenergetics
  • intracellular cations
  • metabolism
  • nuclear magnetic resonance spectroscopy

ASJC Scopus subject areas

  • Physiology
  • Endocrinology
  • Orthopedics and Sports Medicine
  • Physical Therapy, Sports Therapy and Rehabilitation

Cite this

Effects of ischemia on intracellular sodium and phosphates in the in vivo rat liver. / Xia, Zhao Fan; Horton, Jureta W.; Zhao, Pi Yu; Babcock, Evelyn E.; Sherry, A. Dean; Malloy, Craig R.

In: Journal of Applied Physiology, Vol. 81, No. 3, 09.1996, p. 1395-1403.

Research output: Contribution to journalArticle

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AB - Metabolic factors that influence the transition from reversible to irreversible ischemic injury were studied in the rat liver in vivo with 31P-nuclear magnetic resonance (NMR) spectroscopy. Hepatic ischemia for 15, 35, or 65 min was produced by occlusion of the hepatic artery and portal vein in rats. Ischemia caused a rapid decrease in the ATP concentration ([ATP])- to-P(i) concentration ratio and pH within 5 min, but there was little change in these variables detectable by 31P-NMR with longer periods of ischemia. After reperfusion, the [ATP] and P(i) concentration returned toward normal values in livers exposed to 15 or 35 min of ischemia, but 65 min of ischemia were associated with only modest recovery in [ATP], and the [ATP] later decreased. Because the 31P-NMR spectrum was similar after brief compared with prolonged ischemia, it appears that neither ATP depletion, P(i) accumulation, nor acidosis predicts metabolic recovery. Hepatic intracellular Na+ was also measured in separate groups of animals by 23Na-NMR in the presence of a shift agent, thulium (III) 1,4,7,10-tetraazacyclododecane- 1,4,7,10-tetrakis(methylene-phosphonate) (TmDOTP5-), and by atomic absorption spectroscopy. Under baseline conditions, the concentration of intracellular Na+ was 15.2 mM by atomic absorption spectroscopy and 16.5 mM by 23Na-NMR. Although the 31P-NMR spectrum responded very rapidly to the onset of ischemia, intracellular Na+ concentration measured by 23Na-NMR increased gradually but steadily at ~1.0 mM/min during early (up to 15 min) ischemia. These observations demonstrate that a rise in intracellular Na+ does occur during early ischemia, that TmDOTP5- can be applied in vivo for analysis of intracellular Na+ in the ischemic liver, and that 31P-NMR spectroscopy is very sensitive to early ischemic injury.

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