Abstract：
BACKGROUND:The liver is a source of systemic proinflammatory mediators in acute pancreatitis. We have investigated the effects of blood from the pancreas and intestine in liver activation and lung inflammation during early stages of experimental acute pancreatitis in a rat model. METHODS:A portosystemic shunt and a mesosystemic shunt were created to prevent the passage of blood coming from the pancreas and the intestine, respectively, to the liver. Pancreatitis was induced by retrograde injection of 5% sodium taurocholate into the biliopancreatic duct. After 3 hours, the inflammatory process in the lung and intestine, plasma levels of tumor necrosis factor (TNF)-alpha and their soluble receptor, and mRNA expression of inflammatory mediators in the lung were evaluated. RESULTS:Portocaval shunting of blood prevented the inflammatory process in the lung, an increase in plasma TNF-alpha concentration, and the expression of TNF-alpha, interleukin (IL)-1beta, and heat-shock protein (HSP)-72 in the lung, but had no effect on plasma levels of soluble TNF-alpha receptor or on expression of inducible nitric oxide synthase (iNOS) and macrophage inflammatory protein (MIP)-2 in the lung. In contrast, mesocaval shunting of blood did not modify any of the parameters evaluated. CONCLUSIONS:Pancreatic blood, but not intestinal blood, plays a key role in liver activation during experimental acute pancreatitis.
journal_name
Surgeryjournal_title
Surgeryauthors
Hoyos S,Granell S,Heredia N,Bulbena O,Closa D,Fernández-Cruz Ldoi
10.1016/j.surg.2004.06.039subject
Has Abstractpub_date
2005-02-01 00:00:00pages
186-91issue
2eissn
0039-6060issn
1532-7361pii
S0039606004004647journal_volume
137pub_type
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