Groups of anesthetized rats received graded doses of fluoride in isotonic solutions by continuous, iv infusions. Resultant plasma fluoride concentrations included those known to occur in patients following methoxyflurane anesthesia. Graded increases in urine flow rate were not accompanied by increases in sodium or potassium excretion or osmolar clearance. In some experiments, sodium or potassium excretions were reduced, as were urinary osmolality and tubular free water reabsorption. Glomerular filtration rates tended to be reduced in the fluoride infusion groups, while 131I hippuran clearance was not altered. The inner medullary sodium concentration was inversely related to plasma fluoride concentration. Increased renal tissue water content accounted for a portion of slightly reduced medullary potassium concentrations. Histologically, glomeruli from fluoride infused rats contained less than half the erythrocytes of control rat glomeruli. Outer medullary vessels appeared hyperemic. These results suggest that the fluoride induced concentrating defect results from increased medullary blood flow, increased permeability to water, and/or decreased sodium reabsorption, in the ascending limbs of Henle's loops. These findings are consistent with the hypothesis that fluoride is responsible for the concentrating defect following methoxyflurane anesthesia.
ASJC Scopus subject areas
- Anesthesiology and Pain Medicine