To better understand what makes the kidney susceptible to tissue hypoxia, we compared, in the rabbit kidney and hind-limb, the ability of feedback mechanisms governing oxygen consumption (VO(2)) and oxygen delivery (DO(2)) to attenuate tissue hypoxia during hypoxemia. In the kidney (cortex and medulla) and hind-limb (biceps femoris muscle), we determined responses of whole organ blood flow and VO(2), and local perfusion and tissue PO(2), to reductions in DO(2) mediated by graded systemic hypoxemia. Progressive hypoxemia reduced tissue PO(2) similarly in the renal cortex, renal medulla and biceps femoris. Falls in tissue PO(2) could be detected when arterial oxygen content was reduced by as little as 4-8 . VO(2) remained stable during progressive hypoxemia, only tending to fall once arterial oxygen content was reduced by 55 for the kidney or 42 for the hind-limb. Even then, the fall in renal VO(2) could be accounted for by reduced oxygen demand for sodium transport rather than limited oxygen availability. Hind-limb blood flow and local biceps femoris perfusion increased progressively during graded hypoxia. In contrast, neither total renal blood flow nor cortical or medullary perfusion was altered by hypoxemia. Our data suggest that the absence in the kidney of hyperemic responses to hypoxia, and the insensitivity of renal VO2 to limited oxygen availability, contribute to kidney hypoxia during hypoxemia. The susceptibility of the kidney to tissue hypoxia, even in relatively mild hypoxemia, may have important implications for the progression of kidney disease, particularly in patients at high altitude or with chronic obstructive pulmonary disease.
|Pages (from-to)||R931 - R940|
|Number of pages||10|
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|Publication status||Published - 2011|