title: Multiple mechanisms act to maintain kidney oxygenation during renal ischemia in anesthetized rabbits.
abstract: We examined the mechanisms that maintain stable renal tissue PO(2) during moderate renal ischemia, when changes in renal oxygen delivery (DO(2)) and consumption (VO(2)) are mismatched. When renal artery pressure (RAP) was reduced progressively from 80 to 40 mmHg, VO(2) (-38 ± 7%) was reduced more than DO(2) (-26 ± 4%). Electrical stimulation of the renal nerves (RNS) reduced DO(2) (-49 ± 4% at 2 Hz) more than VO(2) (-30 ± 7% at 2 Hz). Renal arterial infusion of angiotensin II reduced DO(2) (-38 ± 3%) but not VO(2) (+10 ± 10%). Despite mismatched changes in DO(2) and VO(2), renal tissue PO(2) remained remarkably stable at ≥40 mmHg RAP, during RNS at ≤2 Hz, and during angiotensin II infusion. The ratio of sodium reabsorption to VO(2) was reduced by all three ischemic stimuli. None of the stimuli significantly altered the gradients in PCO(2) or pH across the kidney. Fractional oxygen extraction increased and renal venous PO(2) fell during 2-Hz RNS and angiotensin II infusion, but not when RAP was reduced to 40 mmHg. Thus reduced renal VO(2) can help prevent tissue hypoxia during mild renal ischemia, but when renal VO(2) is reduced less than DO(2), other mechanisms prevent a fall in renal PO(2). These mechanisms do not include increased efficiency of renal oxygen utilization for sodium reabsorption or reduced washout of carbon dioxide from the kidney, leading to increased oxygen extraction. However, increased oxygen extraction could be driven by altered countercurrent exchange of carbon dioxide and/or oxygen between renal arteries and veins.
authors.affiliation: Dept. of Physiology, PO Box 13F, Monash Univ., Victoria 3800, Australia. Roger.Evans@med.monash.edu.au
authors.forename: Roger G
authors.initials: RG
authors.lastname: Evans
authors.forename: Gabriela A
authors.initials: GA
authors.lastname: Eppel
authors.forename: Sylvia
authors.initials: S
authors.lastname: Michaels
authors.forename: Sandra L
authors.initials: SL
authors.lastname: Burke
authors.forename: Mehdi
authors.initials: M
authors.lastname: Nematbakhsh
authors.forename: Geoffrey A
authors.initials: GA
authors.lastname: Head
authors.forename: Joan F
authors.initials: JF
authors.lastname: Carroll
authors.forename: Paul M
authors.initials: PM
authors.lastname: O'Connor
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D002245:Carbon Dioxide / Q000378:metabolism; D004558:Electric Stimulation; D007511:Ischemia / Q000378:metabolism* / Q000503:physiopathology; D007668:Kidney / Q000098:blood supply* / Q000294:innervation / Q000378:metabolism*; D008297:Male; D023421:Models, Animal; D010100:Oxygen / Q000378:metabolism*; D010101:Oxygen Consumption / Q000187:drug effects / Q000502:physiology; D011817:Rabbits; D051437:Renal Insufficiency / Q000378:metabolism*; D014474:Unconsciousness / Q000378:metabolism* / Q000503:physiopathology; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D000804:Angiotensin II; D002245:Carbon Dioxide; D000109:Acetylcholine; D010100:Oxygen