Acute pancreatitis possible initial triggering mechanism and prophylaxis

Cosen-Binker, Laura Iris; Binker, Marcelo Gustavo; Negri, Gustavo; Tiscornia, Osvaldo

doi:10.1159/000074972

Cited by 14 publications

(28 citation statements)

References 31 publications

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“…Bilio-pancreatic-duct-outlet-exclusion closedduodenal-loops model (BPDOE-CDLs) We described the BPDOE-CDLs model in detail Figure 1, (reproduced with permission granted by the Journal of Pancreatology and S. Karger AG, Basel) [6] . The normally fed animals were anesthetized with sodium pentothal (5 mg/100 g) (Thiopental, Abbott, USA).…”

Section: Methodsmentioning

confidence: 99%

“…Under these circumstances the systemic inflammatory response syndrome (SIRS) may end in a multiorgan dysfunction syndrome (MODS) characterized by metabolic and homodynamic alterations, multifocal organic dysfunction and pluriparenchymatose failure [8] . The bilio-pancreaticduct outlet exclusion closed duodenal loops (BPDOECDLs) model, that we have previously described and validated, mimics these circumstances [6] .…”

Section: R E L a X I N P R E V E N T S T H E D E V E L O P M E N T O mentioning

confidence: 99%

“…Group 2 (surgery control), only underwent the surgical maneuvers involved in triggering AP. Group 3 (AP, BPDOE-CDLs model) acute pancreatitis was triggered by fi lling the closed-duodenal-loops at constant pressure with 8% sodium taurocholate [SIGMA, USA] and 200 uL of methylene blue to corroborate duodenal-refl ux absence [6] . Group 4 (PBS vehicle control and BPDOE-CDLs) acute pancreatitis was induced as for Group 3 and 100 uL PBS were injected sc 1h before and 4 h after the surgery.…”

Section: General Conceptsmentioning

confidence: 99%

“…Inflammatory mediators induce complications that can range from local to systemic evolving to a severe form with high morbi-mortality [2] . The peri-vaterian duodenum (PV-D) has an extremely rich autonomic duodenum-pancreatic inner vation therefore endoscopic maneuvers, gallstones, biliary sludge and/or hemobilia migrating and impacting on the perivaterian duodenum stimulate primary sensory neurons to unchain autonomous-arc-reflexes (AARs) responsible for the initial acute pancreatic neurogenic inflammation that may range from local and edematous to regional and necrotizing pancreatitis [3][4][5][6] . These autonomic nerve fibers are the starting point of autonomic-arc-reflexes which may integrate in the celiac ganglia complex or in the bulbar-hypothalamic autonomous nucleus to end in the intrapancreatic ganglion [6] .…”

Section: Introductionmentioning

confidence: 99%

“…The peri-vaterian duodenum (PV-D) has an extremely rich autonomic duodenum-pancreatic inner vation therefore endoscopic maneuvers, gallstones, biliary sludge and/or hemobilia migrating and impacting on the perivaterian duodenum stimulate primary sensory neurons to unchain autonomous-arc-reflexes (AARs) responsible for the initial acute pancreatic neurogenic inflammation that may range from local and edematous to regional and necrotizing pancreatitis [3][4][5][6] . These autonomic nerve fibers are the starting point of autonomic-arc-reflexes which may integrate in the celiac ganglia complex or in the bulbar-hypothalamic autonomous nucleus to end in the intrapancreatic ganglion [6] . Therefore irritative stimuli induce impulses that travel through thin, unmyelinated, capsaicin-sensitive (type C) nerve fi bers to generate in the somata of the afferent neurons vasoactive peptides such as substance P, neurokinin-A, VIP, SOM and DYN [7] .…”

Section: Introductionmentioning

confidence: 99%

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Relaxin prevents the development of severe acute pancreatitis

Cosen-Binker¹,

Binker²,

Cosen³

et al. 2006

WJG

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AIM:To investigate the severity of acute pancreatitis (AP) is associated to the intensity of leukocyte activation, inflammatory up-regulation and microcirculatory disruption associated to ischemia-reperfusion injury. Microvascular integrity and inhibition of pro-infl ammatory mediators are key-factors in the evolution of AP. Relaxin is an insulin-like hormone that has been attributed vasorelaxant properties via the nitric oxide pathway while behaving as a glucocorticoid receptor agonist. METHODS:AP was induced by the bilio-pancreatic duct-outlet-exclusion closed-duodenal-loops model. Treatment with relaxin was done at different timepoints. Nitric oxide synthase inhibition by L-NAME and glucocorticoid receptor (GR) blockage by mifepristone was considered. AP severity was assessed by biochemical and histopathological analyses. RESULTS:Treatment with relaxin reduced serum amylase, lipase, C-reactive protein, IL-6, IL-10, hsp72, LDH and 8-isoprostane as well as pancreatic and lung myeloperoxidase. Acinar and fat necrosis, hemorrhage and neutrophil infiltrate were also decreased. ATP depletion and ADP/ATP ratio were reduced while caspases 2-3-8 and 9 activities were increased. L-NAME and mifepristone decreased the effi ciency of relaxin. CONCLUSION:Relaxin resulted beneficial in the treatment of AP combining the properties of a GR agonist

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Section: Methodsmentioning

confidence: 99%

Section: R E L a X I N P R E V E N T S T H E D E V E L O P M E N T O mentioning

confidence: 99%

Section: General Conceptsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Relaxin prevents the development of severe acute pancreatitis

Cosen-Binker¹,

Binker²,

Cosen³

et al. 2006

WJG

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Influence of Hydrocortisone, Prednisolone, and NO Association on the Evolution of Acute Pancreatitis

Cosen-Binker

Binker

Cosen³

et al. 2006

Dig Dis Sci

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Leukocyte activation, inflammatory up-regulation, and microcirculatory disruption associated with ischemia-reperfusion injury are hallmarks in the pathogenesis of acute pancreatitis (AP). NO donors ensure microvascular integrity, while glucocorticoids act as anti-inflammatory and immune modulator drugs. AP was induced by the biliopancreatic duct outlet exclusion-closed duodenal loops (BPDOE-CDLs) model. Treatment with hydrocortisone (6 mg/kg) or prednisolone (0.5 mg/kg) alone or together with DETA-NO (0.5 mg/kg) was done (a)1 hr pre or (b)1 hr post, or (c) 1 hr pre and 4 hr post ,or (d) 4 hr post triggering AP. NOS inhibition by L-NAME (15 mg/kg) and glucocorticoid receptor blockage by mifepristone (3 mg/kg) was considered. AP severity was assessed by biochemical and histopathological analyses. Treatment with glucocorticoids together with DETA-NO 1 hr pre and 4 hr post BPDOE-CDLs reduced serum amylase, lipase, C-reactive protein, IL-6, IL-10, hsp72, and 8-isoprostane as well as pancreatic and lung myeloperoxidase. Acinar and fat necrosis, hemorrhage, and neutrophil infiltrate were also decreased. Hydrocortisone together with DETA-NO rendered the best results. We conclude that AP severity was significantly diminished by glucocorticoids associated with DETA-NO, with the optimal dose and time point of administration being crucial to provide adequate protection against AP.

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