Frequency and time course of pancreatic and extrapancreatic bacterial infection in experimental acute pancreatitis in rats☆

Schwarz, Michael; Thomsen, Jens T. W.; Meyer, H.; Büchler, Markus W.; Beger, H. G.

doi:10.1067/msy.2000.104116

Cited by 64 publications

(64 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Intestinal bacterial translocation resulting from the impaired mucosal barrier, microorganism barrier, chemical barrier and immune barrier is an early event [25] and the main cause of infection in SAP [26] . The infection rate of SAP was 30%-50% [27][28][29][30] , leading to a mortality of 40%-80% [31,32] .…”

Section: Discussionmentioning

confidence: 99%

Impact of alanyl-glutamine dipeptide on severe acute pancreatitis in early stage

Xue

Deng²,

Xia³

et al. 2008

WJG

View full text Add to dashboard Cite

INTRODUCTIONAcute pancreatitis (AP) contributes to thousands of annual hospital admissions, of which severe acute pancreatitis (SAP) accounts for 10%-20% [1][2][3] . Despite considerable improvement in the treatment, the mortality of SAP still ranges between 10%-15% [2][3][4][5] . The course of SAP tends to be prolonged and the patients usually are hypermetabolic and high protein catabolic due to systemic inflammatory response syndrome (SIRS) induced by acute local inflammatory process and subsequent vital-organ dysfunction [6] . Thus, if nutritive support is not appropriately administrated to match rapidly increased demand in the treatment of SAP, the patients consequently come down with metabolic disorder and nutrition deficiency, which is considered to increase mortality due to impaired immune function, increased risk of infections and intractable vital-organ failure.In recent years, research showed a conditional deficiency of glutamine would be an independent predictive factor for a poor outcome and its correction improved survival by restoring cellular protective mechanisms, improving immune function and resistance of the gut barrier to hypoperfusion, metabolic stress and subsequent bacterial translocation, and decreasing the risk of infection in critical illness [7][8][9][10] . Since free glutamine is instable in solution, intravenous administration is limited [7] . Alanyl-glutamine METHODS:Eighty patients with SAP were randomized and received 100 mL/d of 20% AGD intravenously for 10 d starting either on the day of (early treatment group) or 5 d after (late treatment group) admission. Groups had similar demographics, underlying diseases, Ranson score, Acute Physiology and Chronic Health Evaluation Ⅱ (APACHE Ⅱ) score, and Balthazar 's computed tomography (CT) score at the beginning of the study and underwent similar other medical and nutritional management. RESULTS:The duration of acute respiratory distress syndrome (2.7 ± 3.3 d vs 12.7 ± 21.0 d, P < 0.01), renal failure (1.3 ± 0.5 d vs 5.3 ± 7.3 d, P < 0.01), acute hepatitis (3.2 ± 2.3 d vs 7.0 ± 7.1 d, P < 0.01), shock (1.7 ± 0.4 d vs 4.8 ± 3.1 d, P < 0.05), encephalopathy (2.3 ± 1.9 d vs 9.5 ± 11.0 d, P < 0.01) and enteroparalysis (2.2 ± 1.4 d vs 3.5 ± 2.2 d, P < 0.01) and hospital stay (28.8 ± 9.4 d vs 45.2 ± 27.1 d, P < 0.01) were shorter in the early treatment group than in the late treatment group. The 15-d APACHE Ⅱ score was lower in the early treatment group than in the late treatment group (5.0 ± 2.4 vs 8.6 ± 3.6, P < 0.01). The infection rate (7.9% vs 26.3%, P < 0.05), operation rate (13.2% vs 34.2%, P < 0.05) and mortality (5.3% vs 21.1%, P < 0.05) in the early treatment group were lower than in the late treatment group.Xue P et al . Impact of AGD on SAP 475 www.wjgnet.com dipeptide (AGD), however, can be taken via vein and hydrolyzed into alanine and glutamine in circulation as a substitute [7] . Presently AGD supplement in parenteral nutrition is a worth-trying approach and an evidence-based recommendation in the management of SAP [11] , but ...

show abstract

Section: Discussionmentioning

confidence: 99%

Impact of alanyl-glutamine dipeptide on severe acute pancreatitis in early stage

Xue

Deng²,

Xia³

et al. 2008

WJG

View full text Add to dashboard Cite

show abstract

“…Meanwhile, the process will further increase intestinal permeability and promote continuous invasion of intestinal bacteria and endotoxin into body to form an infernal circle. Moreover, when intestinal permeability has been increased to certain levels, some macromolecule substances, such as bacteria and lipopolysaccharide, can penetrate the injured intestinal mucosa to move towards multiple organs and lead to a secondary infection of pancreatic tissue (de las Heras et al, 2000;Kazantsev et al, 1994;Gloor et al, 2001;Schwarz et al, 2000), which is the main cause of deaths of AP patients (Carnovale et al, 2005;Furuya et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Mechanism of acute pancreatitis complicated with injury of intestinal mucosa barrier

Zhang

Song

et al. 2007

J. Zhejiang Univ. - Sci. B

View full text Add to dashboard Cite

Acute pancreatitis (AP) is a common acute abdomen in clinic with a rapid onset and dangerous pathogenetic condition.AP can cause an injury of intestinal mucosa barrier, leading to translocation of bacteria or endotoxin through multiple routes, bacterial translocation (BT), gutorigin endotoxaemia, and secondary infection of pancreatic tissue, and then cause systemic inflammatory response syndrome (SIRS) or multiple organ dysfunction syndrome (MODS), which are important factors influencing AP's severity and mortality. Meanwhile, the injury of intestinal mucosa barrier plays a key role in AP's process. Therefore, it is clinically important to study the relationship between the injury of intestinal mucosa barrier and AP. In addition, many factors such as microcirculation disturbance, ischemical reperfusion injury, excessive release of inflammatory mediators and apoptosis may also play important roles in the damage of intestinal mucosa barrier. In this review, we summarize studies on mechanisms of AP.

show abstract

“…While the infusion of 2% taurocholate results in a small necrosis and low mortality, infusion of 5% taurocholate results in fatal pancreatitis within hours. In pancreatitis model of Schwarz et al (23), to get a survey of 36 hours, 3% taurocholate injection was applied and severe necrotizing acute pancreatitisoccurred within 8 hours.In this study, model of pancreatitis generated by Schwarz was preferred and 3% taurocholate solution was infused into the common bile duct. Distinctive fat and parenchymal necrosis was detected in pancreas tissue samples which were taken eight hours after induction of pancreatitis with sacrifi cation of rats.…”

Section: Discussionmentioning

confidence: 99%

Use of infliximab in treatment of acute pancreatitis

Tekin¹,

Teksöz²,

Terzioglu³

et al. 2015

BLL

View full text Add to dashboard Cite

Abstract:Objective: The aim of this study was to investigating the effects of infl iximab in severe necrotizing pancreatitis. Methods: Forty male Wistar rats were randomly divided into fi ve groups evenly. Necrotizing pancreatitis was induced in group I and II by retrograde injection of 3% taurocholate into common pancreaticobiliary duct. In group III and IV saline was introduced instead of taurocholate to mimic pressure effect. Infl iximab (8mg/kg) was infused through tail vein in group I and III and saline was infused in group II and IV just before laparotomy. Group V underwent sham laparotomy. Serum amylase activity, serum and tissue sialic acid, carbonyl content, malondialdehyde, total antioxidant activity (TAA) and pancreatic histopathology were assessed. Results: In group I serum sialic acid, malondialdehyde, carbonyl content and amylase activity were signifi cantly lower than in group II (p<0.01). There were no signifi cant differences for serum TAA between group I and II (p>0.05). Tissue sialic acid and malondialdehyde in group I were signifi cantly lower than in group II (p<0.01). But tissue TAA in group I was signifi cantly higher than in group II (p<0.01). Carbonyl content of group I was not signifi cantly different from group II (p>0.05). Histopathologically, pancreatic sections of group II demonstrated extensive acinar and fat necrosis, hemorrhage, and infl ammation. In group I Infl iximab improved histopathological changes (p<0.01), but not edema (p>0.05). Conclusion: Administration of infl iximab resulted in a signifi cant improvement in biochemical and histopathological alterations in acute necrotizing pancreatitis (Tab. 3, Ref. 43). Text in PDF www.elis.sk.

show abstract

Frequency and time course of pancreatic and extrapancreatic bacterial infection in experimental acute pancreatitis in rats☆

Cited by 64 publications

References 33 publications

Impact of alanyl-glutamine dipeptide on severe acute pancreatitis in early stage

Impact of alanyl-glutamine dipeptide on severe acute pancreatitis in early stage

Mechanism of acute pancreatitis complicated with injury of intestinal mucosa barrier

Use of infliximab in treatment of acute pancreatitis

Contact Info

Product

Resources

About