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dc.contributor.authorPassmore, MR
dc.contributor.authorKi, KK
dc.contributor.authorChan, CHH
dc.contributor.authorLee, T
dc.contributor.authorBouquet, M
dc.contributor.authorWood, ES
dc.contributor.authorRaman, S
dc.contributor.authorRozencwajg, S
dc.contributor.authorBurrell, AJC
dc.contributor.authorMcDonald, CI
dc.contributor.authorLangguth, D
dc.contributor.authorShekar, K
dc.contributor.authorMalfertheiner, MV
dc.contributor.authorFraser, JF
dc.contributor.authorSuen, JY
dc.date.accessioned2020-07-24T04:28:38Z
dc.date.available2020-07-24T04:28:38Z
dc.date.issued2020
dc.identifier.issn0160-564X
dc.identifier.doi10.1111/aor.13771
dc.identifier.urihttp://hdl.handle.net/10072/395744
dc.description.abstractUse of extracorporeal membrane oxygenation (ECMO) is expanding, however it is still associated with significant morbidity and mortality. Activation of inflammatory and innate immune responses and hemostatic alterations contribute to complications. Hyperoxia may play a role in exacerbating these responses. Nine ex vivo ECMO circuits were tested using fresh healthy human whole blood, with two oxygen levels: 21% inspired fraction of oxygen (FiO2 ; mild hyperoxia; n=5) and 100% FiO2 (severe hyperoxia; n=4). Serial blood samples were taken for analysis of platelet aggregometry, leukocyte activation, inflammatory and oxidative stress markers. ECMO resulted in reduced adenosine diphosphate- (p<0.05) and thrombin receptor activating peptide-induced (p<0.05) platelet aggregation, as well as increasing levels of the neutrophil activation marker, neutrophil elastase (p=0.013). Additionally, levels of the inflammatory chemokine interleukin-8 were elevated (p<0.05) and the activity of superoxide dismutase, a marker of oxidative stress, was increased (p=0.002). Hyperoxia did not augment these responses, with no significant differences detected between mild and severe hyperoxia. Our ex vivo model of ECMO revealed that the circuit itself triggers a pro-inflammatory and oxidative stress response however exposure to supra-physiologic oxygen does not amplify that response. Extended-duration studies and inclusion of an endothelial component could be beneficial in characterizing longer-term changes.
dc.description.peerreviewedYes
dc.languageEnglish
dc.language.isoeng
dc.publisherWiley
dc.relation.ispartofjournalArtificial Organs
dc.subject.fieldofresearchBiomedical Engineering
dc.subject.fieldofresearchClinical Sciences
dc.subject.fieldofresearchcode0903
dc.subject.fieldofresearchcode1103
dc.subject.keywordsextracorporeal membrane oxygenation
dc.subject.keywordshyperoxia
dc.subject.keywordsinflammation
dc.subject.keywordsplatelets
dc.titleThe effect of hyperoxia on inflammation and platelet responses in an ex vivo extracorporeal membrane oxygenation circuit
dc.typeJournal article
dc.type.descriptionC1 - Articles
dcterms.bibliographicCitationPassmore, MR; Ki, KK; Chan, CH; Lee, T; Bouquet, M; Wood, ES; Raman, S; Rozencwajg, S; Burrell, AJ; McDonald, CI; Langguth, D; Shekar, K; Malfertheiner, MV; Fraser, JF; Suen, JY, The effect of hyperoxia on inflammation and platelet responses in an ex vivo extracorporeal membrane oxygenation circuit., Artificial Organs, 2020
dc.date.updated2020-07-23T23:55:10Z
dc.description.versionAccepted Manuscript (AM)
gro.rights.copyright© 2020 International Center for Artificial Organs and Transplantation and Wiley Periodicals, Inc. This is the peer reviewed version of the following article: The effect of hyperoxia on inflammation and platelet responses in an ex vivo extracorporeal membrane oxygenation circuit., Artificial Organs, Artificial Organs, 2020, which has been published in final form at https://doi.org/10.1111/aor.13771. This article may be used for non-commercial purposes in accordance with Wiley Terms and Conditions for Self-Archiving (http://olabout.wiley.com/WileyCDA/Section/id-828039.html)
gro.hasfulltextFull Text
gro.griffith.authorFraser, John F.
gro.griffith.authorChan, Hoi Houng


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