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dc.contributor.author
Eshmuminov, Dilmurodjon
dc.contributor.author
Becker, Dustin
dc.contributor.author
Hefti, Max L.
dc.contributor.author
Mueller, Matteo
dc.contributor.author
Hagedorn, Catherine
dc.contributor.author
Dutkowski, Philipp
dc.contributor.author
Rudolf von Rohr, Philipp
dc.contributor.author
Halbe, Maximilian
dc.contributor.author
Segerer, Stephan
dc.contributor.author
Tibbitt, Mark
dc.contributor.author
Bautista Borrego, Lucia
dc.contributor.author
Schuler, Martin J.
dc.contributor.author
Clavien, Pierre-Alain
dc.date.accessioned
2020-12-07T10:32:09Z
dc.date.available
2020-12-07T03:46:09Z
dc.date.available
2020-12-07T10:32:09Z
dc.date.issued
2020
dc.identifier.issn
2045-2322
dc.identifier.other
10.1038/s41598-020-77915-0
en_US
dc.identifier.uri
http://hdl.handle.net/20.500.11850/454852
dc.identifier.doi
10.3929/ethz-b-000454852
dc.description.abstract
Long-term perfusion of liver grafts outside of the body may enable repair of poor-quality livers that are currently declined for transplantation, mitigating the global shortage of donor livers. In current ex vivo liver perfusion protocols, hyperoxic blood (arterial blood) is commonly delivered in the portal vein (PV). We perfused porcine livers for one week and investigated the effect of and mechanisms behind hyperoxia in the PV on hepatic arterial resistance. Applying PV hyperoxia in porcine livers (n = 5, arterial PV group), we observed an increased need for vasodilator Nitroprussiat (285 ± 162 ml/week) to maintain the reference hepatic artery flow of 0.25 l/min during ex vivo perfusion. With physiologic oxygenation (venous blood) in the PV the need for vasodilator could be reduced to 41 ± 34 ml/week (p = 0.011; n = 5, venous PV group). This phenomenon has not been reported previously, owing to the fact that such experiments are not feasible practically in vivo. We investigated the mechanism of the variation in HA resistance in response to blood oxygen saturation with a focus on the release of vasoactive substances, such as Endothelin 1 (ET-1) and nitric oxide (NO), at the protein and mRNA levels. However, no difference was found between groups for ET-1 and NO release. We propose direct oxygen sensing of endothelial cells and/or increased NO break down rate with hyperoxia as possible explanations for enhanced HA resistance.
en_US
dc.format
application/pdf
en_US
dc.language.iso
en
en_US
dc.publisher
Nature Publishing Group
en_US
dc.rights.uri
http://creativecommons.org/licenses/by/4.0/
dc.title
Hyperoxia in portal vein causes enhanced vasoconstriction in arterial vascular bed
en_US
dc.type
Journal Article
dc.rights.license
Creative Commons Attribution 4.0 International
dc.date.published
2020-12-01
ethz.journal.title
Scientific Reports
ethz.journal.volume
10
en_US
ethz.journal.issue
1
en_US
ethz.journal.abbreviated
Sci Rep
ethz.pages.start
20966
en_US
ethz.size
9 p.
en_US
ethz.version.deposit
publishedVersion
en_US
ethz.identifier.wos
ethz.identifier.scopus
ethz.publication.place
London
en_US
ethz.publication.status
published
en_US
ethz.leitzahl
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02130 - Dep. Maschinenbau und Verfahrenstechnik / Dep. of Mechanical and Process Eng.::02668 - Inst. f. Energie- und Verfahrenstechnik / Inst. Energy and Process Engineering::09472 - Tibbitt, Mark / Tibbitt, Mark
ethz.leitzahl.certified
ETH Zürich::00002 - ETH Zürich::00012 - Lehre und Forschung::00007 - Departemente::02130 - Dep. Maschinenbau und Verfahrenstechnik / Dep. of Mechanical and Process Eng.::02668 - Inst. f. Energie- und Verfahrenstechnik / Inst. Energy and Process Engineering::09472 - Tibbitt, Mark / Tibbitt, Mark
ethz.date.deposited
2020-12-07T03:46:15Z
ethz.source
SCOPUS
ethz.eth
yes
en_US
ethz.availability
Open access
en_US
ethz.rosetta.installDate
2020-12-07T10:32:22Z
ethz.rosetta.lastUpdated
2021-02-15T21:29:08Z
ethz.rosetta.exportRequired
true
ethz.rosetta.versionExported
true
ethz.COinS
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