NA-23-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 monitore d using Na-23-NMR in the presence or absence of 1.5 and 15 mM dimethyl thiourea (DMTU) or 15 mM dimethylsulphoxide (DMSO) before and after in ducing hypoxia. Hypoxia induced a prompt exponential increase in total renal Na-23+, renal vascular resistance, and sodium excretion and dec reased inulin clearance and adenine nucleotides and reduced glutathion e concentrations. Lipid peroxide metabolites were unaltered. The incre ase in Na-23+ was significantly reduced (P < 0.001) by both DMTU and D MSO although hypoxic perturbations of function and biochemical paramet ers were not. Posthypoxic increases in renal Na-23+ include approximat ely 10% from the intratubular compartment, but principally reflect the intracellular and interstitial compartments. The results demonstrate that Na-23-NMR is a sensitive indicator of hypoxic renal injury in int act kidney and suggest that DMTU and DMSO protect against hypoxic inju ry by a mechanism independent of free radical-binding.