title: Continuous renal replacement therapy (CRRT) attenuates myocardial inflammation and mitochondrial injury induced by venovenous extracorporeal membrane oxygenation (VV ECMO) in a healthy piglet model.
abstract: In this study, we investigated the myocardial inflammation and mitochondrial function during venovenous extracorporeal membrane oxygenation (VV ECMO) and further evaluated the effects of continuous renal replacement therapy (CRRT) on them. Eighteen piglets were assigned to the control group, ECMO group, and ECMO+CRRT group. Myocardial inflammation was assessed by the activity of myeloperoxidase (MPO), myocardial concentrations, and mRNA expression of TNF-α, IL-1β, and IL-6; mitochondrial function was assessed by activities of mitochondrial complexes I-V. VV ECMO elicited a general activation of serum and myocardial inflammation and significantly decreased the activities of mitochondrial complexes I and IV. After being combined with CRRT, serum and myocardial concentrations of IL-1β and IL-6, myocardial mRNA expression of IL-6, and the activity of MPO were decreased significantly; the activities of mitochondrial complexes were increased. We conclude that myocardial inflammation was activated during ECMO therapy, inducing mitochondrial injury; moreover, CRRT reduced myocardial inflammation and partially ameliorated mitochondrial function.
authors.affiliation: Research Institute of General Surgery, Jinling Hospital, Medical School of Nanjing University, 305 East Zhongshan Road, Nanjing, 210002, Jiangsu, China.
authors.forename: Juanhong
authors.initials: J
authors.lastname: Shen
authors.forename: Wenkui
authors.initials: W
authors.lastname: Yu
authors.forename: Qiyi
authors.initials: Q
authors.lastname: Chen
authors.forename: Jialiang
authors.initials: J
authors.lastname: Shi
authors.forename: Yimin
authors.initials: Y
authors.lastname: Hu
authors.forename: Juanjuan
authors.initials: J
authors.lastname: Zhang
authors.forename: Tao
authors.initials: T
authors.lastname: Gao
authors.forename: Fengchan
authors.initials: F
authors.lastname: Xi
authors.forename: Changsheng
authors.initials: C
authors.lastname: He
authors.forename: Jianfeng
authors.initials: J
authors.lastname: Gong
authors.forename: Ning
authors.initials: N
authors.lastname: Li
authors.forename: Jieshou
authors.initials: J
authors.lastname: Li
mesh_terms: D000818:Animals; D009202:Cardiomyopathies / Q000276:immunology / Q000473:pathology*; D042967:Electron Transport Complex I / Q000378:metabolism; D003576:Electron Transport Complex IV / Q000378:metabolism; D015199:Extracorporeal Membrane Oxygenation / Q000009:adverse effects*; D007249:Inflammation / Q000276:immunology / Q000378:metabolism; D053583:Interleukin-1beta / Q000097:blood / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000097:blood / Q000235:genetics / Q000378:metabolism; D008928:Mitochondria / Q000473:pathology*; D009206:Myocardium / Q000473:pathology; D009195:Peroxidase / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis; D017582:Renal Replacement Therapy / Q000009:adverse effects*; D013552:Swine; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D053583:Interleukin-1beta; D015850:Interleukin-6; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D009195:Peroxidase; D003576:Electron Transport Complex IV; D042967:Electron Transport Complex I