Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/26463
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dc.contributor.authorEvans, Roger G-
dc.contributor.authorCochrane, Andrew D-
dc.contributor.authorHood, Sally G-
dc.contributor.authorIguchi, Naoya-
dc.contributor.authorMarino, Bruno-
dc.contributor.authorBellomo, Rinaldo-
dc.contributor.authorMcCall, Peter R-
dc.contributor.authorOkazaki, Nobuki-
dc.contributor.authorSmith, Julian A-
dc.contributor.authorZhu, Michael Zl-
dc.contributor.authorNgo, Jennifer P-
dc.contributor.authorNoe, Khin M-
dc.contributor.authorMartin, Andrew-
dc.contributor.authorThrift, Amanda G-
dc.contributor.authorLankadeva, Yugeesh R-
dc.contributor.authorMay, Clive N-
dc.date2021-
dc.date.accessioned2021-05-17T05:47:11Z-
dc.date.available2021-05-17T05:47:11Z-
dc.date.issued2021-05-12-
dc.identifier.citationPerfusion 2021; online first: 12 Mayen
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/26463-
dc.description.abstractThe renal medulla is susceptible to hypoxia during cardiopulmonary bypass (CPB), which may contribute to the development of acute kidney injury. But the speed of onset of renal medullary hypoxia remains unknown. We continuously measured renal medullary oxygen tension (MPO2) in 24 sheep, and urinary PO2 (UPO2) as an index of MPO2 in 92 patients, before and after induction of CPB. In laterally recumbent sheep with a right thoracotomy (n = 20), even before CPB commenced MPO2 fell from (mean ± SEM) 52 ± 4 to 41 ±5 mmHg simultaneously with reduced arterial pressure (from 108 ± 5 to 88 ± 5 mmHg). In dorsally recumbent sheep with a medial sternotomy (n = 4), MPO2 was even more severely reduced (to 12 ± 12 mmHg) before CPB. In laterally recumbent sheep in which a crystalloid prime was used (n = 7), after commencing CPB, MPO2 fell abruptly to 24 ±6 mmHg within 20-30 minutes. MPO2 during CPB was not improved by adding donor blood to the prime (n = 13). In patients undergoing cardiac surgery, UPO2 fell by 4 ± 1 mmHg and mean arterial pressure fell by 7 ± 1 mmHg during the 30 minutes before CPB. UPO2 then fell by a further 12 ± 2 mmHg during the first 30 minutes of CPB but remained relatively stable for the remaining 24 minutes of observation. Renal medullary hypoxia is an early event during CPB. It starts to develop even before CPB, presumably due to a pressure-dependent decrease in renal blood flow. Medullary hypoxia during CPB appears to be promoted by hypotension and is not ameliorated by increasing blood hemoglobin concentration.en
dc.language.isoeng
dc.subjectacute kidney injuryen
dc.subjectcardiac surgeryen
dc.subjecthypoxiaen
dc.subjectrenal circulationen
dc.titleDynamic responses of renal oxygenation at the onset of cardiopulmonary bypass in sheep and man.en
dc.typeJournal Articleen
dc.identifier.journaltitlePerfusionen
dc.identifier.affiliationDepartment of Anesthesiology and Resuscitology, Okayama University, Okayama, Japanen
dc.identifier.affiliationDepartment of Anesthesiology and Intensive Care Medicine, Graduate School of Medicine, Osaka University, Osaka, Japanen
dc.identifier.affiliationDepartment of Cardiac Physiology, National Cerebral and Cardiovascular Center Research Institute, Osaka, Japanen
dc.identifier.affiliationAnaesthesiaen
dc.identifier.affiliationIntensive Careen
dc.identifier.affiliationCellsaving and Perfusion Resources, Melbourne, Victoria, Australiaen
dc.identifier.affiliationPre-Clinical Critical Care Unit, Florey Institute of Neuroscience and Mental Health, University of Melbourne, Melbourne, Victoria, Australiaen
dc.identifier.affiliationDepartment of Cardiothoracic Surgery, Monash Health and Department of Surgery (School of Clinical Sciences at Monash Health), Monash University, Melbourne, Victoria, Australiaen
dc.identifier.affiliationCardiovascular Disease Program, Biomedicine Discovery Institute and Department of Physiology, Monash University, Melbourne, Victoria, Australiaen
dc.identifier.affiliationDepartment of Medicine, School of Clinical Sciences at Monash Health, Monash University, Melbourne, Victoria, Australiaen
dc.identifier.doi10.1177/02676591211013640en
dc.type.contentTexten
dc.identifier.orcid0000-0002-9241-0757en
dc.identifier.orcid0000-0001-9980-9640en
dc.identifier.pubmedid33977810
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