Oxygen Pressure in Urine and Its Relation to Intrarenal Blood Flow

Abstract

Oxygen tensions in renal pelvic urine, renal venous blood and arterial blood ( Pu, Pv, Pa) were measured in anesthetized dogs breathing oxygen tensions of 150, 760 and 1900 mm Hg. In dogs having high Diodrast extraction ratios, the respective values for Pu were 27, S.E. ± 3; 49 ± 5 and 120 ± 7 mm Hg. Corresponding values for Pv were 50 ± 3, 96 ± 8 and 858 ± 47 mm Hg. Renal O2 consumption was unaffected by oxygen tension; therefore, the increasing Pv– Pu cannot be interpreted as a gradient across tubule cells. In dogs having low Diodrast extraction ratios, Pu was higher (e.g. 72 ± 6 mm Hg in contrast to 49 ± 5 at 1 atm. O2). These results, which are difficult to explain by classical renal hemodynamics, can be accounted for by the cell-separation theory. Assuming that urine oxygen is equilibrated with peritubular capillary blood it is possible to calculate peritubular relative to arterial hematocrit ( HT/ Ha). HT/ Ha, so calculated, averages 0.52 ± .06 for high extraction kidneys and 0.96 ± .06 for low extraction kidneys, thus relating low Diodrast extraction to failure of cell-separation. An alternative mechanism, involving equilibration of urine oxygen with medullary, rather than peritubular, blood could also explain the facts provided that the hematocrit of medullary blood is low. Further work is required to localize the region of low oxygen tension within the kidney: the present results indicate, however, that the region concerned is supplied with blood of low red cell concentration. Oxygen in human bladder urine is largely determined by gaseous equilibration with ureteral walls and cannot be used as a measure of intrarenal oxygen pressure.