Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/32353
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dc.contributor.authorElsaafien, Khalid-
dc.contributor.authorSloan, Jasmine M-
dc.contributor.authorEvans, Roger G-
dc.contributor.authorCochrane, Andrew D-
dc.contributor.authorMarino, Bruno-
dc.contributor.authorMcCall, Peter R-
dc.contributor.authorHood, Sally G-
dc.contributor.authorYao, Song T-
dc.contributor.authorKorim, Willian S-
dc.contributor.authorBailey, Simon R-
dc.contributor.authorJufar, Alemayehu H-
dc.contributor.authorPeiris, Rachel M-
dc.contributor.authorBellomo, Rinaldo-
dc.contributor.authorMiles, Lachlan F-
dc.contributor.authorMay, Clive N-
dc.contributor.authorLankadeva, Yugeesh R-
dc.date2023-
dc.date.accessioned2023-03-22T02:18:48Z-
dc.date.available2023-03-22T02:18:48Z-
dc.date.issued2023-04-01-
dc.identifier.citationAnesthesia and Analgesia 2023; 136(4): 802-813en_US
dc.identifier.issn1526-7598-
dc.identifier.urihttps://ahro.austin.org.au/austinjspui/handle/1/32353-
dc.description.abstractIntraoperative inflammation may contribute to postoperative neurocognitive disorders after cardiac surgery requiring cardiopulmonary bypass (CPB). However, the relative contributions of general anesthesia (GA), surgical site injury, and CPB are unclear. In adult female sheep, we investigated (1) the temporal profile of proinflammatory and anti-inflammatory cytokines and (2) the extent of microglia activation across major cerebral cortical regions during GA and surgical trauma with and without CPB (N = 5/group). Sheep were studied while conscious, during GA and surgical trauma, with and without CPB. Plasma tumor necrosis factor-alpha (mean [95% confidence intervals], 3.7 [2.5-4.9] vs 1.6 [0.8-2.3] ng/mL; P = .0004) and interleukin-6 levels (4.4 [3.0-5.8] vs 1.6 [0.8-2.3] ng/mL; P = .029) were significantly higher at 1.5 hours, with a further increase in interleukin-6 at 3 hours (7.0 [3.7-10.3] vs 1.8 [1.1-2.6] ng/mL; P < .0001) in animals undergoing CPB compared with those that did not. Although cerebral oxygen saturation was preserved throughout CPB, there was pronounced neuroinflammation as characterized by greater microglia circularity within the frontal cortex of sheep that underwent CPB compared with those that did not (0.34 [0.32-0.37] vs 0.30 [0.29-0.32]; P = .029). Moreover, microglia had fewer branches within the parietal (7.7 [6.5-8.9] vs 10.9 [9.4-12.5]; P = .001) and temporal (7.8 [7.2-8.3] vs 9.9 [8.2-11.7]; P = .020) cortices in sheep that underwent CPB compared with those that did not. CPB enhanced the release of proinflammatory cytokines beyond that initiated by GA and surgical trauma. This systemic inflammation was associated with microglial activation across 3 major cerebral cortical regions, with a phagocytic microglia phenotype within the frontal cortex, and an inflammatory microglia phenotype within the parietal and temporal cortices. These data provide direct histopathological evidence of CPB-induced neuroinflammation in a large animal model and provide further mechanistic data on how CPB-induced cerebral inflammation might drive postoperative neurocognitive disorders in humans.en_US
dc.language.isoeng-
dc.titleAssociations Between Systemic and Cerebral Inflammation in an Ovine Model of Cardiopulmonary Bypass.en_US
dc.typeJournal Articleen_US
dc.identifier.journaltitleAnesthesia and Analgesiaen_US
dc.identifier.affiliationPre-Clinical Critical Care Unit, Florey Institute of Neuroscience and Mental Health.en_US
dc.identifier.affiliationDepartment of Cardiothoracic Surgery, Monash Health, and Department of Surgery (School of Clinical Sciences at Monash Health), Monash University, Melbourne, Victoria, Australia.en_US
dc.identifier.affiliationCellsaving and Perfusion Resources, Melbourne, Victoria, Australia.en_US
dc.identifier.affiliationAnaesthesiaen_US
dc.identifier.affiliationCardiovascular Neuroscience Laboratory, Department of Anatomy and Physiology, University of Melbourne, Melbourne, Victoria, Australia.en_US
dc.identifier.affiliationFaculty of Veterinary Science, University of Melbourne, Melbourne, Victoria, Australia.en_US
dc.identifier.affiliationDepartment of Critical Care, Melbourne Medical School, Melbourne, Victoria, Australiaen_US
dc.identifier.affiliationclinicalen_US
dc.identifier.doi10.1213/ANE.0000000000006379en_US
dc.type.contentTexten_US
dc.identifier.pubmedid36928157-
dc.description.volume136-
dc.description.issue4-
dc.description.startpage802-
dc.description.endpage813-
dc.subject.meshtermssecondaryCardiopulmonary Bypass/adverse effects-
dc.subject.meshtermssecondaryInflammation/etiology-
local.name.researcherBellomo, Rinaldo
item.languageiso639-1en-
item.fulltextNo Fulltext-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.cerifentitytypePublications-
item.openairetypeJournal Article-
crisitem.author.deptAnaesthesia-
crisitem.author.deptIntensive Care-
crisitem.author.deptData Analytics Research and Evaluation (DARE) Centre-
crisitem.author.deptAnaesthesia-
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