The serum levels of pro-inflammatory cytokines.

<p>Increases in interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-α (TNF-α) generation at 12 and 24 h after induction of severe acute pancreatitis (SAP). These increases in cytokine levels were significantly ameliorated by regional arterial infusion (RAI) with Asprin-Triggered Lipoxin A₄ (ATL) (<i>P</i><0.01). Seven rats were studied in each experimental group at each time point. The results are expressed as means and SD. * <i>P</i><0.05 and ** <i>P</i><0.01, ATL vs. the SAP group.</p

Immunofluorescence staining for ICAM-1 and PECAM-1 in the pancreas.

<p><b>A)</b> The expression of ICAM-1 in vascular endothelial cells in the pancreas increased after induction of severe acute pancreatitis (SAP) compared to the sham group; findings significantly attenuated by regional arterial infusion (RAI) with Asprin-Triggered Lipoxin A₄ (ATL). <b>C)</b> Fluorescence intensity for ICAM-1. The results are expressed as means and SD. The mean fluorescence intensity of ICAM-1 decreased significantly in the ATL group both at 12 and 24 h (<i>P</i><0.05 vs. SAP). <b>B)</b> The expression of PECAM-1 in vascular endothelial cells in the pancreas increased significantly after induction of SAP compared to the sham group, attenuated by RAI with ATL. <b>D)</b> Bar graph demonstrating fluorescence intensity for PECAM-1. The results are expressed as means and SD. The mean fluorescence intensity of PECAM-1 decreased significantly in the ATL group both at 12 and 24 h (<i>P</i><0.05). * <i>P</i><0.05 and ** <i>P</i><0.01, ATL vs. the SAP group.</p

The scores of pathological grading of pancreatic injury and pancreatic index.

<p>SAP = severe acute pancreatitis.</p><p>ATL = SAP+regional arterial infusion ATL.</p><p><i>P</i> value = the statistical value of the SAP vs. the ATL group.</p><p>The scores of pathological grading of pancreatic injury and pancreatic index.</p

Western blot analysis of heme oxygenase-1 (HO-1), NF-κB p65, ICAM-1 and PECAM-1 in the pancreas.

<p><b>A)</b> Representative photographs of HO-1 protein levels in the pancreas in the three groups. <b>E)</b> Bar graph quantifying the HO-1 protein level in the pancreas. HO-1 protein levels in the pancreas increased after induction of severe acute pancreatitis (SAP) compared to the sham group, significantly increased following regional arterial infusion with Asprin-Triggered Lipoxin A₄ (ATL) (<i>P</i><0.01 vs. SAP). <b>B)</b> Representative photographs of nuclear NF-κB protein level in the pancreas in the three groups. <b>F)</b> Bar graph quantifying nuclear NF-κB protein levels in the pancreas. Protein levels of nuclear NF-κB in the pancreas increased after induction of SAP compared to the sham group, and decreased significantly in the ATL group both at 12 and 24 h (<i>P</i><0.05 or <i>P</i><0.01, respectively, vs. SAP). <b>C)</b> Representative photographs of ICAM-1 protein levels in the pancreas in the three groups. <b>G)</b> Bar graph quantifying ICAM-1 protein levels in the pancreas, increased after induction of SAP as compared to the sham group, and significantly decreased in the ATL group (<i>P</i><0.05 vs. SAP). <b>D)</b> Representative photographs of PECAM-1 protein levels in the pancreas in the three groups. <b>H)</b> Bar graph quantifying PECAM-1 protein levels in the pancreas, increased after induction of SAP (vs. sham) and significantly decreased in the ATL group both at 12 and 24 h (<i>P</i><0.05 vs. SAP). The results are expressed as means and SD. * <i>P</i><0.05 and ** <i>P</i><0.01, ATL vs. the SAP group.</p

The weight of ascetic, serum levels of amylase and PLA₂, and MPO activity in pancreas.

<p><b>A)</b> The weight of ascitic fluid increased after induction of severe acute pancreatitis (SAP), though without significant difference after regional arterial infusion (RAI) with Asprin-Triggered Lipoxin A₄ (ATL). <b>B)</b> The amylase activity increased rapidly in the SAP group both at 12 and 24 h compared to the sham group and decreased significantly after RAI with ATL (<i>P</i><0.05). <b>C)</b> Serum levels of PLA₂ (ELISA) increased in the SAP group vs. the sham group, higher at 24 h than at 12 h both in the SAP and ATL groups. PLA₂ serum levels in the ATL group decreased (<i>P</i><0.05 vs. SAP). <b>D)</b> MPO levels in the pancreas increased after SAP induction, significantly attenuated after RAI with ATL both at 12 and 24 h (<i>P</i><0.05 and <i>P</i><0.01, respectively). Seven rats were studied in each experimental group at each time point. The results are expressed as means and SD. * <i>P</i><0.05 and ** <i>P</i><0.01, ATL group vs. the SAP group.</p

Representative photographs of HE stained pancreas.

<p>Pathological section of pancreatic tissue under light microscope (HE staining × 100). The sham group (A and D) was normal. Tissue edema, inflammatory cell infiltration, hemorrhage, and necrosis in the pancreas were observed in the severe acute pancreatitis (SAP) group (B and E). Changes were substantially ameliorated by regional arterial infusion (RAI) with Asprin-Triggered Lipoxin A₄ (ATL) (Fig. C and F).</p

Reduced Pancreatic Exocrine Function and Organellar Disarray in a Canine Model of Acute Pancreatitis

<div><p>The aim of the present study was to investigate the pancreatic exocrine function in a canine model and to analyze the changes in organelles of pancreatic acinar cells during the early stage of acute pancreatitis (AP). AP was induced by retrograde injection of 5% sodium taurocholate (0.5 ml/kg) into the main pancreatic duct of dogs. The induction of AP resulted in serum hyperamylasemia and a marked reduction of amylase activity in the pancreatic fluid (PF). The pancreatic exocrine function was markedly decreased in subjects with AP compared with the control group. After the induction of AP, histological examination showed acinar cell edema, cytoplasmic vacuolization, fibroblasts infiltration, and inflammatory cell infiltration in the interstitium. Electron micrographs after the induction of AP revealed that most of the rough endoplasmic reticulum (RER) were dilated and that some of the ribosomes were no longer located on the RER. The mitochondria were swollen, with shortened and broken cristae. The present study demonstrated, in a canine model, a reduced volume of PF secretion with decreased enzyme secretion during the early stage of AP. Injury of mitochondria and dilatation and degranulation of RER may be responsible for the reduced exocrine function in AP. Furthermore, the present model and results may be useful for researching novel therapeutic measures in AP.</p></div

The PF volume, outputs of amylase activity, lipase activity, and protein concentration in the PF in a canine AP model.

<p>AP was induced by a retrograde injection of 5% sodium taurocholate (0.5 ml/kg) via the main pancreatic duct. (A): volume of PF (ml/24 h), (B): amylase activity in PF (U/l), (C): lipase activity in PF (U/l), (D): protein concentration in PF (g/l), (n = 6 dogs per group). The PF volume, amylase activity, lipase activity, and protein concentration in the PF were significantly decreased after the induction of AP compared with the control group. *P < 0.05, the AP group vs. the control group at both time points.</p

Composition of TPN Formulation.

<p>Composition of TPN Formulation.</p

Bicarbonate concentration and pH value in the PF in a canine AP model.

<p>AP was induced by a retrograde injection of 5% sodium taurocholate (0.5 ml/kg) via the main pancreatic duct. (A) Bicarbonate concentration in the PF, (B) pH value of the PF, (n = 6 dogs per group). The bicarbonate concentration and pH value in the PF were significantly decreased after AP induction compared with the control group. *P < 0.05, the AP group vs. the control group at both time points.</p