title: Lidocaine Administration Controls MicroRNAs Alterations Observed After Lung Ischemia-Reperfusion Injury.
abstract: Ischemia-reperfusion injury (IRI) is associated with morbidity and mortality. MicroRNAs (miRNAs) have emerged as regulators of IRI, and they are involved in the pathogenesis of organ rejection. Lidocaine has proven anti-inflammatory activity in several tissues but its modulation of miRNAs has not been investigated. This work aims to investigate the involvement of miRNAs in lung IRI in a lung auto-transplantation model and to investigate the effect of lidocaine.
  
  
  
  Three groups (sham, control, and Lidocaine), each comprising 6 pigs, underwent a lung autotransplantation. All groups received the same anesthesia. In addition, animals of lidocaine group received a continuous intravenous administration of lidocaine (1.5 mg/kg/h) during surgery. Lung biopsies were taken before pulmonary artery clamp, before reperfusion, 30 minutes postreperfusion (Rp-30), and 60 minutes postreperfusion (Rp-60). Samples were analyzed for different miRNAs (miR-122, miR-145, miR-146a, miR-182, miR-107, miR-192, miR-16, miR-21, miR-126, miR-127, miR142-5p, miR152, miR155, miR-223, and let7) via the use of reverse-transcription quantitative polymerase chain reaction. Results were normalized with miR-103.
  
  
  
  The expression of miR-127 and miR-16 did not increase after IRI. Let-7d, miR-21, miR-107, miR-126, miR-145, miR-146a, miR-182, and miR-192 significantly increased at the Rp-60 (control versus sham P < .001). miR-142-5p, miR-152, miR-155, and miR 223 significantly increased at the Rp-30 (control versus sham P < .001) and at the Rp-60 (control versus. sham P < .001). The administration of lidocaine was able to attenuate these alterations in a significant way (control versus Lidocaine P < .001).
  
  
  
  Lung IRI caused dysregulation miRNA. The administration of lidocaine reduced significantly miRNAs alterations.
authors.affiliation: From the *Department of Biochemistry and Molecular Biology III, Faculty of Medicine, Complutense University of Madrid, Spain; Departments of †Thoracic Surgery and ‡Anesthesiology, Hospital Gregorio Marañón, Madrid, Spain; and Departments of §Physiology and ‖Biostatistics and Operational Investigation, Faculty of Medicine, Complutense University of Madrid, Spain.
authors.forename: Lisa
authors.initials: L
authors.lastname: Rancan
authors.forename: Carlos
authors.initials: C
authors.lastname: Simón
authors.forename: Emmeline
authors.initials: E
authors.lastname: Marchal-Duval
authors.forename: Javier
authors.initials: J
authors.lastname: Casanova
authors.forename: Sergio Damian
authors.initials: SD
authors.lastname: Paredes
authors.forename: Alberto
authors.initials: A
authors.lastname: Calvo
authors.forename: Cruz
authors.initials: C
authors.lastname: García
authors.forename: David
authors.initials: D
authors.lastname: Rincón
authors.forename: Agustín
authors.initials: A
authors.lastname: Turrero
authors.forename: Ignacio
authors.initials: I
authors.lastname: Garutti
authors.forename: Elena
authors.initials: E
authors.lastname: Vara
mesh_terms: D000818:Animals; D051017:Apoptosis Regulatory Proteins / Q000378:metabolism; D004195:Disease Models, Animal; D005786:Gene Expression Regulation; D018836:Inflammation Mediators / Q000378:metabolism; D008012:Lidocaine / Q000494:pharmacology*; D008168:Lung / Q000187:drug effects* / Q000378:metabolism; D055370:Lung Injury / Q000188:drug therapy* / Q000209:etiology / Q000235:genetics / Q000378:metabolism; D016040:Lung Transplantation / Q000009:adverse effects; D008297:Male; D035683:MicroRNAs / Q000235:genetics / Q000378:metabolism*; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000209:etiology / Q000235:genetics / Q000378:metabolism; D034421:Sus scrofa; D013997:Time Factors; D014182:Transplantation, Autologous / Q000009:adverse effects
chemical_list: D051017:Apoptosis Regulatory Proteins; D018836:Inflammation Mediators; D035683:MicroRNAs; D008012:Lidocaine