title: Mechanisms of the beneficial effect of hypertonic saline solution in acute pancreatitis.
abstract: Administration of hypertonic saline (HS) solution to rats with acute pancreatitis (AP) decreases mortality and systemic inflammation. We hypothesized that these effects are related not only to systemic inflammatory reduction, but also to a reduction of the pancreatic lesion. Acute pancreatitis was induced in Wistar rats by injection of 2.5% sodium taurocholate. Animals were divided in groups: without AP, not treated AP, AP treated with NaCl 0.9%, and AP treated with NaCl 7.5%. Trypsinogen activation peptides and amylase activity were increased in ascitic fluid and serum and were not affected by treatment with HS. Pancreatic inflammation was evaluated by increased myeloperoxidase activity, malondialdehyde formation, and histopathology for severity of pancreatic lesions. The HS did not affect these parameters. Expression of cyclooxygenase 2 and inducible nitric oxide synthase was markedly increased in the pancreas of the AP group and was reduced by treatment with HS. This treatment also reduced the levels of TNF-α and IL-6 but not of IL-10 in the pancreatic tissue. These results show that HS modulates cytokine production and expression of enzymes responsible for inflammatory mediator production in the pancreas without affecting the severity of the pancreatic lesions.
authors.affiliation: Department of Gastroenterology (LIM/37), Medical School, University of Sao Paulo, Sao Paulo, Brazil.
authors.forename: Ana Maria Mendonça
authors.initials: AM
authors.lastname: Coelho
authors.forename: José
authors.initials: J
authors.lastname: Jukemura
authors.forename: Sandra N
authors.initials: SN
authors.lastname: Sampietre
authors.forename: Joilson O
authors.initials: JO
authors.lastname: Martins
authors.forename: Nilza A T
authors.initials: NA
authors.lastname: Molan
authors.forename: Rosely A
authors.initials: RA
authors.lastname: Patzina
authors.forename: Björn
authors.initials: B
authors.lastname: Lindkvist
authors.forename: Sonia
authors.initials: S
authors.lastname: Jancar
authors.forename: José Eduardo M
authors.initials: JE
authors.lastname: Cunha
authors.forename: Luiz A Carneiro
authors.initials: LA
authors.lastname: D'Albuquerque
authors.forename: Marcel Cerqueira Cesar
authors.initials: MC
authors.lastname: Machado
mesh_terms: D000208:Acute Disease; D000681:Amylases / Q000097:blood; D000818:Animals; D001201:Ascites / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000032:analysis; D004353:Drug Evaluation, Preclinical; D016753:Interleukin-10 / Q000032:analysis; D015850:Interleukin-6 / Q000032:analysis; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D009504:Neutrophils / Q000201:enzymology; D052247:Nitric Oxide Synthase Type II / Q000032:analysis; D009842:Oligopeptides / Q000032:analysis; D010195:Pancreatitis / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D009195:Peroxidase / Q000032:analysis; D051381:Rats; D017208:Rats, Wistar; D012462:Saline Solution, Hypertonic / Q000494:pharmacology*; D013656:Taurocholic Acid / Q000633:toxicity; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D015850:Interleukin-6; D009842:Oligopeptides; D012462:Saline Solution, Hypertonic; D014409:Tumor Necrosis Factor-alpha; C080396:trypsinogen activation peptide; D016753:Interleukin-10; D013656:Taurocholic Acid; D009195:Peroxidase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D051546:Cyclooxygenase 2; C489691:Ptgs2 protein, rat; D000681:Amylases