Sarre,1 in 1938, observed a consistently lower oxygen pressure (Po2) in the urine than in renal-vein blood. Twenty years later, this finding was confirmed by Reeves et al2 who attributed the disparity to the cell-separation, plasma-skimming mechanism proposed by Pappenheimer and Kinter.3 According to this concept, the urinary oxygen pressure (Puo2) is controlled by renal hemodynamic factors. The rapid blood flow through the long straight interlobular arteries results in a midstream concentration of red blood cells and a marginal sheath of low-hematocrit plasma. The afferent glomerular arterioles, which take off at right angles from the interlobular arteries, are fed from the periphery of the stream. Thus each tier of glomeruli, from the deep to the outer cortex, receives blood of increasingly higher hematocrit. The renal medulla, which derives its blood supply from the efferent arterioles of the juxtamedullary glomeruli (the vasa recta), therefore receives cell-poor,
Leonhardt KO, Landes RR. Urinary Oxygen Pressure in Renal Parenchymal and Vascular Disease: Effects of Breathing Oxygen. JAMA. 1965;194(4):345–350. doi:10.1001/jama.1965.03090170023008
Customize your JAMA Network experience by selecting one or more topics from the list below.
Create a personal account or sign in to: