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dc.contributor.authorPischke, Søren
dc.contributor.authorHestenes, Siv Merete
dc.contributor.authorJohansen, Harald Thidemann
dc.contributor.authorFure, Hilde
dc.contributor.authorBugge, Jan F
dc.contributor.authorEspinoza, Andreas Westenvik
dc.contributor.authorSkulstad, Helge
dc.contributor.authorEdvardsen, Thor
dc.contributor.authorFosse, Erik
dc.contributor.authorMollnes, Tom Eirik
dc.contributor.authorHalvorsen, Per Steinar
dc.contributor.authorNielsen, Erik Waage
dc.identifier.citationPLOS ONE. 2019, 14:e0218624 (6), 1-16.nb_NO
dc.description.abstractIntroduction Right ventricular (RV) myocardial dysfunction is a common feature in septic shock. It can worsen outcome, but the etiology is poorly understood. Pulmonary artery hypertension (PAH) plays a part in the pathogenesis of the right heart dysfunction in sepsis but its importance is unknown. In pigs, PAH in sepsis is substantial and the translational value of porcine sepsis models therefore questioned. We hypothesized that porcine sepsis causes a myocardial inflammatory response which leads to myocardial dysfunction independent of PAH. Materials and methods Sepsis was induced by Escherichia coli-infusion in 10 pigs resulting in PAH and increased right ventricular pressure (RVP). The same degree of RVP was achieved by external pulmonary artery banding (PAB) in a consecutive series of 6 animals. Results Sepsis, but not PAB, led to increase in endothelial damage marker PAI-1 and cytokines TNF and IL-6 (all p<0.05) in plasma. In myocardium, TNF and IL-6 were significantly elevated in sepsis, TNF in both ventricles and IL-6 mostly in RV, while IL-1β, IL-18 and C5a were significantly higher in RV compared to LV after PAB (all p<0.05). Myocardial mRNA levels of IL-1β, IL-6, IL-18, IP-10, E-selectin and PAI-1 were significantly elevated in RV and LV during sepsis compared to PAB, while Caspase-1 was decreased in septic compared to PAB animals (all p<0.05). Cathepsin L activity was increased in RV by PAB, while sepsis inhibited this response. Escherichia coli-induced sepsis caused myocardial inflammation independent of PAH. Conclusion Prominent PAH should therefore not exclude porcine sepsis models to further our understanding of human sepsis.nb_NO
dc.publisherPublic Library of Sciencenb_NO
dc.rightsNavngivelse 4.0 Internasjonal*
dc.titleSepsis causes right ventricular myocardial inflammation independent of pulmonary hypertension in a porcine sepsis modelnb_NO
dc.typeJournal articlenb_NO
dc.typePeer reviewednb_NO
dc.source.journalPLOS ONEnb_NO
dc.description.localcode© 2019 Pischke et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are creditednb_NO
cristin.unitnameInstitutt for klinisk og molekylær medisin

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