title: Severe acute pancreatitis: a possible role of intramyocardial cytokine production.
abstract: BACKGROUND
  Several mechanisms are involved in the development of the local and systemic response in acute pancreatitis. Cardiovascular system may be affected throughout the clinical course of acute pancreatitis. The aim was to evaluate local myocardial cytokine production, as well as, functional and histological myocardial alterations in severe acute pancreatitis.
  
  
  METHODS
  The animals were divided into three groups: Group 1: control; Group 2: sham; Group 3: severe acute pancreatitis. Echocardiographic assessment of cardiac function, serum levels of amylase and cytokines (TNF-α, IL-6 and IL-10), and mRNA expression of TNF-α, IL-6 and TGF-β were measured. Myocardial tissue alterations were analysed by histological examination.
  
  
  RESULTS
  The serum TNF-α and IL-10 levels were significant higher in AP 2h group. The mRNA IL-6 levels from group AP 2h were statistically higher. The mRNA TNF-α level from sham group and AP 2h were statistically lower. Significant changes in the left ventricular diameter were found in AP 2h and AP 12h groups. There were statistical changes for vacuolar degeneration, picnosis and loss of nucleus, and lymphocytes.
  
  
  CONCLUSIONS
  We found cardiac and histological changes compatible with the inflammatory process triggered by SAP with the promotion of local myocardial cytokine production.
authors.affiliation: Department of Gastroenterology (LIM-37), School of Medicine, University of São Paulo, São Paulo, Brazil. alberto.meyer@usp.br.
authors.forename: Alberto
authors.initials: A
authors.lastname: Meyer
authors.forename: Márcia S
authors.initials: MS
authors.lastname: Kubrusly
authors.forename: Vera M
authors.initials: VM
authors.lastname: Salemi
authors.forename: Ana M
authors.initials: AM
authors.lastname: De Mendonça Coelho
authors.forename: Nilza A T
authors.initials: NA
authors.lastname: Molan
authors.forename: Roseli A
authors.initials: RA
authors.lastname: Patzina
authors.forename: Marcel C C
authors.initials: MC
authors.lastname: Machado
authors.forename: Charles
authors.initials: C
authors.lastname: Mady
authors.forename: Luiz A C
authors.initials: LA
authors.lastname: D'Albuquerque
authors.forename: José
authors.initials: J
authors.lastname: Jukemura
mesh_terms: D000208:Acute Disease; D000681:Amylases / Q000097:blood; D000818:Animals; D001706:Biopsy; D016207:Cytokines / Q000235:genetics / Q000276:immunology* / Q000378:metabolism; D004452:Echocardiography; D006331:Heart Diseases / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D006334:Heart Function Tests; D018836:Inflammation Mediators / Q000097:blood; D016753:Interleukin-10 / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D008297:Male; D009206:Myocardium / Q000276:immunology* / Q000378:metabolism; D010195:Pancreatitis / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism; D017208:Rats, Wistar; D012720:Severity of Illness Index; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000276:immunology / Q000378:metabolism
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D015850:Interleukin-6; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D000681:Amylases