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23 Na‐NMR detects hypoxic injury in intact kidney: Increases in sodium inhibited by DMSO and DMTU
Author(s) -
Cross M.,
Endre Z. H.,
StewartRichardson P.,
Cowin G. J.,
Westhuyzen J.,
Duggleby R. G.,
Fleming S. J.
Publication year - 1993
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.1910300409
Subject(s) - sodium , chemistry , isotopes of sodium , kidney , nuclear magnetic resonance , radiochemistry , nuclear chemistry , medicine , physics , organic chemistry
Hypoxic injury in the isolated perfused rat kidney (IPRK) was monitored using 23 Na‐NMR in the presence or absence of 1.5 and 15 m M dimethylthiourea (DMTU) or 15 mM dimethylsulphoxide (DMSO) before and after inducing hypoxia. Hypoxia induced a prompt exponential increase in total renal 23 Na+, renal vascular resistance, and sodium excretion and decreased inulin clearance and adenine nucleotides and reduced glutathione concentrations. Lipid peroxide metabolites were unaltered. The increase in 23 Na+ was significantly reduced ( P < 0.001) by both DMTU and DMSO although hypoxic perturbations of function and biochemical parameters were not. Posthypoxic increases in renal 23 Na + include approximately 10% from the intratubular compartment, but principally reflect the intracellular and interstitial compartments. The results demonstrate that 23Na‐NMR is a sensitive indicator of hypoxic renal injury in intact kidney and suggest that DMTU and1 DMSO protect against hypoxic injury by a mechanism independent of free radical‐binding.