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Acute Necrotizing Pancreatitis (acute + necrotizing_pancreatitis)

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Medical Sciences100%

Selected Abstracts

Use of activated protein C has no avail in the early phase of acute pancreatitis

HPB, Issue 6 2008
Sinan Akay
Abstract Objectives. Sepsis and acute pancreatitis have similar pathogenetic mechanisms that have been implicated in the progression of multiple organ failure. Drotrecogin alfa, an analogue of endogenous protein C, reduces mortality in clinical sepsis. Our objective was to evaluate the early therapeutic effects of activated protein C (APC) in a rat model of acute necrotizing pancreatitis. Subjects and method. Acute necrotizing pancreatitis was induced by intraductal injection of 5% Na taurocholate. Hourly bolus injections of saline or recombinant human APC (drotrecogin alfa) was commenced via femoral venous catheter four hours after the induction of acute pancreatitis. The experiment was terminated nine hours after pancratitis induction. Animals in group one (n=20) had a sham operation while animals in group two (n=20) received saline and animals in group three (n=20) received drotrecogin alfa boluses after acute pancreatitis induction. Pancreatic tissue for histopathologic scores and myeloperoxidase, glutathione reductase, glutathione peroxidase, and catalase activites were collected, and blood for serum amylase, urea, creatinine, and inleukin-6 measurements was withdrawn. Results. Serum amylase activity was significantly lower in the APC treated group than the untreated group (17,435±432 U/L vs. 27,426±118 U/L, respectively). While the serum interleukin-6 concentration in the APC untreated group was significantly lower than the treated group (970±323 pg/mL vs. 330±368 pg/mL, respectively). Conclusion. In the early phase of acute pancreatitis, drotrecogin alfa treatment did not result in a significant improvement in oxidative and inflammatory parameters or renal functions. [source]

Beneficial effects of growth hormone on bacterial translocation during the course of acute necrotizing pancreatitis in rats

JOURNAL OF DIGESTIVE DISEASES, Issue 1 2001
Wang Xingpeng
OBJECTIVE: Because bacterial translocation from the gut is one of the important sources of bacterial infection in acute necrotizing pancreatitis (ANP), and growth hormone (GH) has the ability to promote intestinal epithelial proliferation, we investigated the effects of GH on bacterial translocation in a rat ANP model. METHODS: Acute necrotizing pancreatitis was induced in rats via injection of 5% sodium taurocholate into the biliopancreatic duct. The rats with ANP were treated with either human recombinant GH or a placebo. Laparotomized animals without ANP induction (sham operation) served as controls. Twenty-four hours after the operation, blood was drawn for bacterial culture and determinations of amylase, lipase and endotoxin. Peritoneal fluid and specimens of mesenteric lymph nodes (MLN), liver, pancreas and spleen were taken for bacterial culture by standard techniques. Intestinal mucosal permeability was assessed by measuring the movement of [125I]-labeled albumin from blood to the intestinal lumen. Insulin-like growth factor-1 (IGF-1) mRNA was detected in the liver and ileum by reverse transcription,polymerase chain reaction (RT-PCR). Morphological changes in the pancreas and ileum were also analyzed. RESULTS: Administration of GH significantly decreased the activity of serum amylase and lipase, decreased the plasma endotoxin level and reduced the incidence of bacterial translocation. Moreover, the survival rate of ANP rats was improved. The severity of inflammation in the pancreas and ileum was reduced by GH treatment. Ileal mucosal thickness, villus height and crypt depth in GH-treated rats were obviously increased as compared with those of ANP rats. The intestinal permeability was markedly decreased in the GH group as compared with the ANP group. GH treatment resulted in upregulation of IGF-1 mRNA expression in ileum, but not in liver. CONCLUSIONS: These results suggest that exogenous GH has beneficial effects in maintaining the integrity of the intestinal mucosal barrier and reducing the incidence of bacterial translocation in rats with ANP. One of the mechanisms might be the upregulation of IGF-1 mRNA in the intestine by GH. [source]

Use of activated protein C has no avail in the early phase of acute pancreatitis

HPB, Issue 6 2008
Sinan Akay
Abstract Objectives. Sepsis and acute pancreatitis have similar pathogenetic mechanisms that have been implicated in the progression of multiple organ failure. Drotrecogin alfa, an analogue of endogenous protein C, reduces mortality in clinical sepsis. Our objective was to evaluate the early therapeutic effects of activated protein C (APC) in a rat model of acute necrotizing pancreatitis. Subjects and method. Acute necrotizing pancreatitis was induced by intraductal injection of 5% Na taurocholate. Hourly bolus injections of saline or recombinant human APC (drotrecogin alfa) was commenced via femoral venous catheter four hours after the induction of acute pancreatitis. The experiment was terminated nine hours after pancratitis induction. Animals in group one (n=20) had a sham operation while animals in group two (n=20) received saline and animals in group three (n=20) received drotrecogin alfa boluses after acute pancreatitis induction. Pancreatic tissue for histopathologic scores and myeloperoxidase, glutathione reductase, glutathione peroxidase, and catalase activites were collected, and blood for serum amylase, urea, creatinine, and inleukin-6 measurements was withdrawn. Results. Serum amylase activity was significantly lower in the APC treated group than the untreated group (17,435±432 U/L vs. 27,426±118 U/L, respectively). While the serum interleukin-6 concentration in the APC untreated group was significantly lower than the treated group (970±323 pg/mL vs. 330±368 pg/mL, respectively). Conclusion. In the early phase of acute pancreatitis, drotrecogin alfa treatment did not result in a significant improvement in oxidative and inflammatory parameters or renal functions. [source]

Beneficial effects of growth hormone on bacterial translocation during the course of acute necrotizing pancreatitis in rats

JOURNAL OF DIGESTIVE DISEASES, Issue 1 2001
Wang Xingpeng
OBJECTIVE: Because bacterial translocation from the gut is one of the important sources of bacterial infection in acute necrotizing pancreatitis (ANP), and growth hormone (GH) has the ability to promote intestinal epithelial proliferation, we investigated the effects of GH on bacterial translocation in a rat ANP model. METHODS: Acute necrotizing pancreatitis was induced in rats via injection of 5% sodium taurocholate into the biliopancreatic duct. The rats with ANP were treated with either human recombinant GH or a placebo. Laparotomized animals without ANP induction (sham operation) served as controls. Twenty-four hours after the operation, blood was drawn for bacterial culture and determinations of amylase, lipase and endotoxin. Peritoneal fluid and specimens of mesenteric lymph nodes (MLN), liver, pancreas and spleen were taken for bacterial culture by standard techniques. Intestinal mucosal permeability was assessed by measuring the movement of [125I]-labeled albumin from blood to the intestinal lumen. Insulin-like growth factor-1 (IGF-1) mRNA was detected in the liver and ileum by reverse transcription,polymerase chain reaction (RT-PCR). Morphological changes in the pancreas and ileum were also analyzed. RESULTS: Administration of GH significantly decreased the activity of serum amylase and lipase, decreased the plasma endotoxin level and reduced the incidence of bacterial translocation. Moreover, the survival rate of ANP rats was improved. The severity of inflammation in the pancreas and ileum was reduced by GH treatment. Ileal mucosal thickness, villus height and crypt depth in GH-treated rats were obviously increased as compared with those of ANP rats. The intestinal permeability was markedly decreased in the GH group as compared with the ANP group. GH treatment resulted in upregulation of IGF-1 mRNA expression in ileum, but not in liver. CONCLUSIONS: These results suggest that exogenous GH has beneficial effects in maintaining the integrity of the intestinal mucosal barrier and reducing the incidence of bacterial translocation in rats with ANP. One of the mechanisms might be the upregulation of IGF-1 mRNA in the intestine by GH. [source]

Experimental pancreatitis disturbs gastrointestinal and colonic motility in mice: effect of the prokinetic agent tegaserod

NEUROGASTROENTEROLOGY & MOTILITY, Issue 10 2007
T. C. Seerden
Abstract, Acute pancreatitis remains a potentially life-threatening disease associated with gastrointestinal motility disturbances. Prokinetic agents may be useful to overcome these motility disturbances. In this study, we investigated the effect of acute necrotizing pancreatitis (ANP) on gastrointestinal motility in female mice and evaluated the effect of tegaserod, a prokinetic 5-hydroxytryptamine-4 (5HT4) receptor agonist. ANP was induced by feeding mice a choline-deficient ethionine-supplemented diet during 72 h. In vivo intestinal motility was measured as the geometric centre (GC) of 25 glass beads 30-120-360 min after gavage. Colonic peristaltic activity was studied using a modified Trendelenburg set-up. ANP significantly decreased GC 30-120-360 min after bead gavage, associated with a significant increase of myeloperoxidase in the proximal small intestine and colon, but not in the stomach or distal small intestine. Tegaserod significantly ameliorated GC 360 min after bead gavage in control and pancreatitis mice. In isolated colonic segments, ANP significantly decreased the amplitude of peristaltic waves and increased the interval between peristaltic contractions. Tegaserod normalized the disturbed interval. In conclusion, ANP impairs gastric, small intestinal and colonic motility in mice. Tegaserod improves ANP-induced motility disturbances in vivo and in vitro, suggesting a therapeutic benefit of prokinetic 5HT4 receptor agonists in the treatment of pancreatitis-induced ileus. [source]