23Na-NMR detects hypoxic injury in intact kidney: increases in sodium inhibited by DMSO and DMTU

• Published in: Magnetic resonance in medicine Vol. 30; no. 4; p. 465
• Main Authors: Cross, M, Endre, Z H, Stewart-Richardson, P, Cowin, G J, Westhuyzen, J, Duggleby, R G, Fleming, S J
• Format: Journal Article
• Language: English
• Published: United States 01.10.1993
• Subjects: Animals; Dimethyl Sulfoxide - therapeutic use; Hypoxia - complications; Kidney Diseases - etiology; Kidney Diseases - metabolism; Magnetic Resonance Spectroscopy; Male; Rats; Rats, Wistar; Sodium - metabolism; Thiourea - analogs & derivatives; Thiourea - therapeutic use
• ISSN: 0740-3194
• DOI: 10.1002/mrm.1910300409

Hypoxic injury in the isolated perfused rat kidney (IPRK) was monitored using 23Na-NMR in the presence or absence of 1.5 and 15 mM dimethylthiourea (DMTU) or 15 mM dimethylsulphoxide (DMSO) before and after inducing hypoxia. Hypoxia induced a prompt exponential increase in total renal 23Na+, 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 23Na+ 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 23Na+ 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 and DMSO protect against hypoxic injury by a mechanism independent of free radical-binding.