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Evaluation of extra‐ and intracellular apparent diffusion coefficient of sodium in rat skeletal muscle: Effects of prolonged ischemia
Author(s) -
Babsky Andriy M.,
Topper Stephen,
Zhang Hong,
Gao Yong,
James Judy R.,
Hekmatyar Shahryar K.,
Bansal Navin
Publication year - 2008
Publication title -
magnetic resonance in medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.696
H-Index - 225
eISSN - 1522-2594
pISSN - 0740-3194
DOI - 10.1002/mrm.21568
Subject(s) - sodium , extracellular , ischemia , chemistry , skeletal muscle , intracellular , extracellular fluid , diffusion , in vivo , nuclear magnetic resonance , biophysics , medicine , biochemistry , biology , thermodynamics , physics , microbiology and biotechnology , organic chemistry
The mechanism of water and sodium apparent diffusion coefficient (ADC) changes in rat skeletal muscle during global ischemia was examined by in vivo 1 H and 23 Na magnetic resonance spectroscopy (MRS). The ADCs of Na + and water are expected to have similar characteristics because sodium is present as an aqua‐cation in tissue. The shift reagent, TmDOTP 5‐ , was used to separate intra‐ and extracellular sodium (Na i +and Na e + , respectively) signals. Water, total tissue sodium (Na t + ), Na i + , and Na e +ADCs were measured before and 1, 2, 3, and 4 hr after ischemia. Contrary to the general perception, Na i +and Na e +ADCs were identical before ischemia. Thus, ischemia‐induced changes in Na t +ADC cannot be explained by a simple change in the size of relative intracellular or extracellular space. Na t +and Na e +ADCs decreased after 2–4 hr of ischemia, while water and Na i +ADC remained unchanged. The correlation between Na t +and Na e +ADCs was observed because of high Na e +concentration. Similarly, the correlation between water and Na i +ADCs was observed because cells occupy 80% of the tissue space in the skeletal muscle. Ischemia also caused an increase in the Na i +and an equal decrease in Na e +signal intensity due to cessation of Na + /K + ‐ATPase function. Magn Reson Med 59:485–491, 2008. © 2008 Wiley‐Liss, Inc.