PloS one, 2019-06, Vol.14 (6), p.e0218624-e0218624
2019
Details
- Autor(en) / Beteiligte
- Titel
- Sepsis causes right ventricular myocardial inflammation independent of pulmonary hypertension in a porcine sepsis model
- Ist Teil von
- PloS one, 2019-06, Vol.14 (6), p.e0218624-e0218624
- Ort / Verlag
- United States: Public Library of Science
- Erscheinungsjahr
- 2019
- Link zum Volltext
- Quelle
- EZB Free E-Journals
- Beschreibungen/Notizen
- 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. 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. 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. Prominent PAH should therefore not exclude porcine sepsis models to further our understanding of human sepsis.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1932-6203eISSN: 1932-6203DOI: 10.1371/journal.pone.0218624Titel-ID: cdi_plos_journals_2248368044
- Format
- –
- Schlagworte
- Anesthesiology, Animal models, Animals, Bacteria, Basale medisinske, odontologiske og veterinærmedisinske fag: 710, Basic medical, dental and veterinary science disciplines: 710, Biology and Life Sciences, Cardiology, Cardiomyopathy, Caspase-1, Cathepsin L, Cathepsins, Critical care, Cytokines, Cytokines - blood, Cytokines - genetics, Disease Models, Animal, E coli, E-selectin, EDTA, Emergencies, Endothelium, Etiology, Etiology (Medicine), External pressure, Female, Health sciences, Heart, Heart diseases, Hospitals, Hypertension, Hypertension, Pulmonary - complications, Hypertrophy, Right Ventricular - etiology, Hypertrophy, Right Ventricular - pathology, IL-1β, Immunology, Infection, Inflammation, Inflammatory response, Intensive care, Interleukin 18, Interleukin 6, IP-10 protein, Laboratories, Lungs, Male, Medical disciplines: 700, Medical research, Medicine, Medicine and Health Sciences, Medicine, Experimental, Medisinske Fag: 700, Messenger RNA, Mortality, mRNA, Myocarditis - etiology, Myocarditis - genetics, Myocarditis - pathology, Myocardium, Myocardium - metabolism, Myocardium - pathology, Pathogenesis, Physiology, Plasminogen Activator Inhibitor 1 - blood, Pulmonary arteries, Pulmonary artery, Pulmonary hypertension, Research and Analysis Methods, Risk factors, RNA, RNA, Messenger - genetics, RNA, Messenger - metabolism, Sepsis, Sepsis - blood, Sepsis - complications, Sepsis - genetics, Septic shock, Shock, Sus scrofa, Swine, Systematic review, Tumor necrosis factor, VDP, Ventricle, Ventricular Dysfunction, Right - etiology, Ventricular Dysfunction, Right - pathology