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

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.