CO2 abdominal insufflation decreases local and systemic inflammatory response in experimental acute pancreatitis.
OBJECTIVE
Acute pancreatitis (AP) is a serious disease that is amplified by an associated systemic inflammatory response. We investigated the effect of CO2 pneumoperitoneum on the local and systemic inflammatory response in AP.


METHODS
Acute pancreatitis was induced in Wistar rats by 5% taurocholate intraductal injection. Carbon dioxide pneumoperitoneum was applied for 30 minutes before the induction of AP. Inflammatory parameters were evaluated in the peritoneum (ascites, cell number, and tumor necrosis factor alpha [TNF-alpha]), serum (amylase, TNF-alpha, interleukin-6 [IL-6], and IL-10), pancreas (myeloperoxidase [MPO] activity, cyclo-oxygenase 2 and inducible nitric oxide synthase expression, and histological diagnosis), liver, and lung (mitochondria dysfunction and MPO activity).


RESULTS
Abdominal insufflation with CO2 before induction of AP caused a significant decrease in ascites volume, cells, and TNF-alpha in the peritoneal cavity and in serum TNF-alpha and IL-6 but not IL-10 levels. In the pancreas, this treatment reduced MPO activity, acinar and fat necrosis, and the expression of inducible nitric oxide synthase and cyclo-oxygenase 2. There were no significant differences on serum amylase levels, liver mitochondrial function, and pulmonary MPO between groups.


CONCLUSIONS
Our data demonstrated that CO2 pneumoperitoneum reduced pancreatic inflammation and attenuated systemic inflammatory response in AP. This article suggests that CO2 pneumoperitoneum plays a critical role on the better outcome in patients undergoing laparoscopic pancreatic surgery.
Machado
Marcel Cerqueira Cesar
MC
Department of Gastroenterology, and daggerMedical School and Immunology, Institute of Biomedical Sciences, University of São Paulo, São Paulo, Brazil.
Coelho
Ana Maria Mendonça
AM
Martins
Joilson O
JO
Sampietre
Sandra N
SN
Molan
Nilza A T
NA
Patzina
Rosely A
RA
Machado
Marcel Autran Cesar
MA
Jancar
Sonia
S
D000681:Amylases / Q000097:blood; D000818:Animals; D001201:Ascites / Q000276:immunology / Q000517:prevention & control; D002245:Carbon Dioxide / Q000008:administration & dosage*; D051546:Cyclooxygenase 2 / Q000378:metabolism; D004195:Disease Models, Animal; D018836:Inflammation Mediators / Q000097:blood; D007327:Insufflation; D016753:Interleukin-10 / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D008168:Lung / Q000276:immunology; D008297:Male; D008930:Mitochondria, Liver / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D010084:Oxidation-Reduction; D010085:Oxidative Phosphorylation; D010179:Pancreas / Q000201:enzymology / Q000276:immunology* / Q000473:pathology; D010195:Pancreatitis / Q000139:chemically induced / Q000201:enzymology / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D009195:Peroxidase / Q000378:metabolism; D011028:Pneumoperitoneum, Artificial; D051381:Rats; D017208:Rats, Wistar; D018746:Systemic Inflammatory Response Syndrome / Q000201:enzymology / Q000276:immunology / Q000473:pathology / Q000517:prevention & control*; D013656:Taurocholic Acid; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
D018836:Inflammation Mediators; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D002245:Carbon Dioxide; D013656:Taurocholic Acid; D009195:Peroxidase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D051546:Cyclooxygenase 2; C489691:Ptgs2 protein, rat; D000681:Amylases