Sepsis causes right ventricular myocardial inflammation independent of pulmonary hypertension in a porcine sepsis model
AuthorPischke, Søren; Hestenes, Siv Merete; Johansen, Harald Thidemann; Fure, Hilde; Bugge, Jan F; Espinoza, Andreas Westenvik; Skulstad, Helge; Edvardsen, Thor; Fosse, Erik; Mollnes, Tom Eirik; Halvorsen, Per Steinar; Nielsen, Erik Waage
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.