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Renal medullary tissue oxygenation is dependent on both cortical and medullary blood flow

Department of Physiology, Monash University, Melbourne, Victoria, Australia

Submitted 6 July 2005 ; accepted in final form 7 October 2005

The aim of the current study was to determine whether renal medullary oxygenation is independent of the level of cortical blood flow by testing responses to stimuli that selectively reduce blood flow in either the cortex or medulla. In anesthetized rabbits, renal arterial infusion of [Phe²,Ile³,Orn⁸]-vasopressin selectively reduced medullary perfusion and PO₂ (–54 ± 24 and –50 ± 10%, respectively) but did not significantly affect cortical perfusion or tissue oxygenation. In contrast, stimulation of the renal nerves resulted in renal cortical ischemia with reductions in total renal blood flow (–76 ± 3% at 4 Hz), cortical perfusion (–57 ± 17%), and cortical PO₂ (–44 ± 12%). Medullary tissue PO₂ was reduced by –70 ± 5% at 4 Hz, despite medullary perfusion being unaffected and distal tubular sodium reabsorption being reduced (by –83.3 ± 1.2% from baseline). In anesthetized rats, in which renal perfusion pressure was maintained with an aortic constrictor, intravenous infusion of ANG II (0.5–5 µg·kg^–1·min^–1) dose dependently reduced cortical perfusion (up to –65 ± 3%; P < 0.001) and cortical PO₂ (up to –57 ± 4%; P < 0.05). However, medullary perfusion was only significantly reduced at the highest dose (5 µg·kg^–1·min^–1; by 29 ± 6%). Medullary perfusion was not reduced by 1 µg·kg^–1·min^–1 ANG II, but medullary PO₂ was significantly reduced (–12 ± 4%). Thus, although cortical and medullary blood flow may be independently regulated, medullary oxygenation may be compromised during moderate to severe cortical ischemia even when medullary blood flow is maintained.

acute renal failure; acute tubular necrosis; hypoxia; ischemia; laser-Doppler flowmetry; fluorescence oximetry; oxygen; rabbits; rats; renal circulation

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