Acute pancreatitis possible initial triggering mechanism and prophylaxis

doi:10.1159/000074972

Pancreatology

Volume 3, Issue 6, 2003, Pages 445-456

https://doi.org/10.1159/000074972 Get rights and content

Abstract

Background and Aims: Biliary acute pancreatitis or postendoscopic iatrogenia acute pancreatitis (AP) are likely triggered by autonomous arc reflexes (AAR) initiated in the peri-Vaterian duodenum (PV-D). The bilio-pancreatic duct outlet exclusion closed duodenal loops (BPDOE-CDL) model mimics these circumstances. Our aim was to validate this model and evaluate the role of AAR via their interruption with local anesthetics. Methods: Severe AP was induced in Wistar rats with the BPDOE-CDL model: extra-pancreatic insult was provoked in the PV-D by distension with 8% sodium taurocholate and methylene blue for 45 min to show the absence of duodenum pancreatic reflux. Treated experimental groups received a 2% lidocaine chlorhydrate gel instilled into the PV-D prior to triggering the AP, or before and after at the celiac-ganglia complex, or at both sites. The degree of severity was evaluated using biochemical and histopath-ological analysis. Results: Induction of AP by BPDOE-CDL was severe, with acinar and fat necrosis and hemorrhage with a greater foci number in the cephalic segment. Groups pretreated with local anesthetic developed mild or moderate AP characterized by edema and leukocyte infiltrate. Serum amylase, lipase and CRP were significantly reduced in all treated groups. Other blood metabolites and pancreatic myeloperoxidase, amylase and lipase, were significantly decreased. Conclusion: The BPDOE-CDL model was validated, emphasizing the importance of AAR as extrapancreatic initiators of AP. The interruption of AAR by lidocaine chlorhydrate prevented excessive pancreatic inflammation and diminished hemorrhage and necrosis and may prove a useful prophylactic procedure to prevent postendoscopic severe AP.

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²: Supported by a research grant given to Laura Iris Cosen-Binker by GlaxoSmithKline S.A.

¹: Laura Iris Cosen-Binker, BD, PhD, Research Institute — Hospital for Sick Children, 555 University Avenue-Room 10112, Elm Wing — Toronto, Ont. M5G 1X8 (Canada), Tel./Fax +1 416 925 9069

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Acute pancreatitis possible initial triggering mechanism and prophylaxis2

Abstract

J Biol Chem

Food Chem Toxicol

Pancreatology

Gastroenterol

J Gas-trointest Surg

Am J Surg

Gastroenterology

Blood

Some aspects of human and canine macroscopic pancreas innervation

Am J Gastroenterol

Síntesis conceptual de la inervación macroscopica gastro-duodeno-pancreática

Ac Ge La

Relación funcional antro-duodeno pancreática. Parte I

Acta Gastroenterol Latinoam

Relación funcional antro-duodeno pancreáitica. Parte II

Acta Gastroenterol Latinoam

Neurology and neuropathology of the pancreatic innervation. JOP

Pancreas Online J

Diagnostic relevance on interleukin pattern and acute-phase proteins in early phase of post-ERCP pancreatitis

Dig Dis Sci

Peut-on prévenis la pancréatite aiguë apres cathétérisme endoscopique bilio-pancréatique?

Hepatogastro

Clinical outcome of post-ERCP pancreatitis: Relationship to history of previous pancreatitis

Am J Gastroenterol

Pancreatitis secondary to percutaneous liver biopsy-associated hemobilia

Am J Gastroenterol

ERCP and endoscopic sphincterotomy-induced pancreatitis

Pancreas

Vasoactive mediators and the progression from oedematous to necrotizing experimental acute pancreatitis

Gut

Hemodynamic Disorders, Thrombosis and Shock

Mediators of ischemia-reperfusion injury of rat lung

Am J Physiol

Oxidative stress in acute pancreatitis

Hepato-Gastroenterology

Tissue-specific cytokine production during experimental acute pancreatitis: A probable mechanism for distant organ dysfunction

Dig Dis Sci

Physiopathologie de l’inflammation pancréatique au cours de la pancréatite aiguë

Hepatogastro

Pulmonary infiltrations sign of severe acute pancreatitis

Int J Pancreatol

Leukotriene generation and neutrophil infiltration after experimental acute pancreatitis

Inflammation

Acute pancreatitis and cytokines, ‘second attack’ by septic complication leads to organ failure

Pancreas