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dc.contributor.authorOw, CPC
dc.contributor.authorNgo, JP
dc.contributor.authorUllah, MM
dc.contributor.authorBarsha, G
dc.contributor.authorMeex, RCR
dc.contributor.authorWatt, MJ
dc.contributor.authorHilliard, LM
dc.contributor.authorKoeners, MP
dc.contributor.authorEvans, RG
dc.date.accessioned2018-12-04T11:54:46Z
dc.date.issued2018-10-29
dc.description.abstractTissue hypoxia has been proposed as an important event in renal ischemia reperfusion injury (IRI) particularly during the period of ischemia and in the immediate hours following reperfusion. However, little is known about renal oxygenation during the subacute phase of IRI. We employed four different methods to assess the temporal and spatial changes in tissue oxygenation during the subacute phase (24 h and 5 days after reperfusion) of a severe form of renal IRI in rats. We hypothesized that the kidney is hypoxic 24 h and 5 days after an hour of bilateral renal ischemia, driven by a disturbed balance between renal oxygen delivery (DO2) and oxygen consumption (VO2). Renal DO2 was not significantly reduced in the subacute phase of IRI. In contrast, renal VO2 was 55% less 24 h, and 49% less 5 days after reperfusion than after sham-ischemia. Inner medullary tissue PO2, measured by radiotelemetry was 25 {plus minus} 12% greater 24 h after ischemia than after sham-ischemia. By 5 days after reperfusion, tissue PO2 was similar to that in rats subjected to sham-ischemia. Tissue PO2 measured by Clark electrode was consistently greater 24 h, but not 5 days, after ischemia than after sham-ischemia. Cellular hypoxia, assessed by pimonidazole adduct immunohistochemistry, was largely absent at both time-points and tissue levels of hypoxia inducible factors were downregulated following renal ischemia. Thus, in this model of severe IRI, tissue hypoxia does not appear to be an obligatory event during the subacute phase, likely due to the markedly reduced oxygen consumption.en_GB
dc.description.sponsorshipBritish Heart Foundationen_GB
dc.description.sponsorshipBritish Heart Foundationen_GB
dc.description.sponsorshipNational Health and Medical Research Council of Australiaen_GB
dc.description.sponsorshipEuropean Union, Seventh Framework Programmeen_GB
dc.identifier.citationVol. 315 (5), pp. F1358-F1369en_GB
dc.identifier.doi10.1152/ajprenal.00249.2018
dc.identifier.grantnumberFS/14/2/30360en_GB
dc.identifier.grantnumberPG/15/68/31717en_GB
dc.identifier.grantnumberGNT606601en_GB
dc.identifier.grantnumberGNT1024575en_GB
dc.identifier.grantnumberGNT1077703en_GB
dc.identifier.grantnumber612280en_GB
dc.identifier.grantnumber282821en_GB
dc.identifier.urihttp://hdl.handle.net/10871/34983
dc.language.isoenen_GB
dc.publisherAmerican Physiological Societyen_GB
dc.relation.urlhttps://www.ncbi.nlm.nih.gov/pubmed/30110566en_GB
dc.rights© 2018 the American Physiological Society. Open access. Licensed under Creative Commons Attribution CC-BY 4.0 : © the American Physiological Society.en_GB
dc.subjectacute kidney injuryen_GB
dc.subjecthypoxiaen_GB
dc.subjectischemia reperfusionen_GB
dc.subjectkidneyen_GB
dc.subjectoxygenen_GB
dc.titleAbsence of renal hypoxia in the subacute phase of severe renal ischemia reperfusion injuryen_GB
dc.typeArticleen_GB
dc.date.available2018-12-04T11:54:46Z
exeter.place-of-publicationUnited Statesen_GB
dc.description This is the author accepted manuscript. The final version is available from American Physiological Society via the DOI in this recorden_GB
dc.identifier.journalAJP - Renal Physiologyen_GB
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/deed.en_USen_GB
dcterms.dateAccepted2018-08-09
exeter.funder::British Heart Foundationen_GB
exeter.funder::British Heart Foundationen_GB
rioxxterms.versionAMen_GB
rioxxterms.licenseref.startdate2018-10-29
rioxxterms.typeJournal Article/Reviewen_GB
refterms.dateFCD2018-12-04T11:49:37Z
refterms.versionFCDAM
refterms.dateFOA2019-02-18T13:01:19Z
refterms.panelAen_GB


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© 2018 the American Physiological Society. Open access.

Licensed under Creative Commons Attribution CC-BY 4.0 : © the American Physiological Society.
Except where otherwise noted, this item's licence is described as © 2018 the American Physiological Society. Open access. Licensed under Creative Commons Attribution CC-BY 4.0 : © the American Physiological Society.