Prostaglandin E&lt;sub&gt;1&lt;/sub&gt;Treatment in Experimental Acute Pancreatitis in the Rat

Crocket, K.V.; Brackett, Kim A.; Crocket, Aysel; Jacobson, Eugene D.; Rao, Sambasiva; Joffe, Stephen N.

doi:10.1159/000128418

Cited by 4 publications

(2 citation statements)

References 14 publications

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“…Recent studies have demonstrated a number of treatments that have an effect on both the course and severity of acute pancreatitis. These include protease inhibitors 131, 132 , trypsin inhibitors 134–136, somatostatin 137 , prostaglandin E 1 138 , vasopressin 139 and dextran 40 140 .…”

Section: Invasive Experimental Modelsmentioning

confidence: 99%

Review of experimental animal models of acute pancreatitis

Cuthbertson

Christophi

2006

HPB

134

105

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The underlying mechanisms involved in the pathogenesis of acute pancreatitis are ill understood. The mortality rate of this disease has not significantly improved over the past few decades. Current treatment options are limited, and predominantly aimed at supportive therapy. A key feature of severe acute pancreatitis is the presence of extensive tissue necrosis with both local and systemic manifestations of inflammatory response syndromes. A better understanding of the underlying pathophysiology of severe acute pancreatitis may lead to more targeted therapeutic options, potentially leading to improved survival. Animal models of acute pancreatitis are therefore an essential investigative tool for these aims to be achieved. This review discusses the suitability of recent non-invasive models of acute pancreatitis such as hormone-induced, alcohol-induced, immune-mediated, diet-induced, gene knockout and L-arginine; and invasive models including closed duodenal loop, antegrade pancreatic duct perfusion, biliopancreatic duct injection, combination of secretory hyperstimulation with minimal intraductal bile acid exposure, vascular-induced, ischaemia/reperfusion and duct ligation.

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Section: Invasive Experimental Modelsmentioning

confidence: 99%

Review of experimental animal models of acute pancreatitis

Cuthbertson

Christophi

2006

HPB

134

105

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“…Findings from this model support the hypothesis that reflux of duodenal contents into the pancreatic duct is a possible etiologic factor in the development of acute pancreatitis (Su, Cuthbertson, and Christophi 2006). While ligation of the duodenum is ultimately lethal, the model has efficacy with a number of treatments that affect both the course and severity of the ensuing pancreatitis including the coadministration of protease inhibitors (Murakami et al 1990; Ono et al 1990), somatostatin (De Rai et al 1988), prostaglandin E1 (Crocket et al 1984), and vasopressin (Schapiro et al 1976).…”

Section: Animal Models Of Acute Pancreatitismentioning

confidence: 99%

A Review of Animal Models of Nonneoplastic Pancreatic Diseases

Foster

2013

Toxicol Pathol

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The nonneoplastic diseases of the human pancreas generally comprise the inflammatory and degenerative conditions that include acute and chronic pancreatitis, with cystic fibrosis being arguably one of the most important diseases that induce the condition. Both acute and chronic conditions vary in severity, but both can be life threatening; and because of this fact, the study of their progression, and their responsiveness to therapy, is largely conducted by indirect means using serum markers of damage and repair such as amylase and lipase activities that normally occur at very low levels in the circulation but can be significantly increased during inflammatory episodes. Progress in the understanding the pathogenesis of both conditions has therefore been largely due to time course studies in animal models of pancreatitis, and it is in this context that animal model development has been so significant. In general terms, the animal models can be divided into the invasive, surgical procedures, and those induced by the administration of chemical secretagogues that induce hypersecretion of the pancreatic enzymes. The former include ligation and/or cannulation of the biliopancreatic ducts with infusion of solutions of various kinds, or the formation of closed duodenal loops. Secretagogue administration includes administration of caerulein or l-arginine in various protocols. An additional model involves administration of dibutyltin dichloride, which induces a partial blockage of the pancreatic ducts to induce pancreatic disease through enzymic reflux into the gland. The models have been invaluable in generating testable hypotheses for the human diseases. These hypotheses for the production of cellular damage as the initiating events in the disease include (1) intracellular chemical activation, (2) pancreatic secretion reflux, (3) intracellular production of reactive oxygen species, and (4) intracellular production of free radicals.

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