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Updated: Jul 11, 2026

Establishment of a Mouse Severe Acute Pancreatitis Model using Retrograde Injection of Sodium Taurocholate into the Biliopancreatic Duct
Published on: April 1, 2022
Nitric oxide pathways and evidence-based perturbations in acute pancreatitis
1Department of Internal Medicine, Division of Gastroenterology and Hepatology, University of Michigan School of Medicine, Ann Arbor, MI 48109, USA. mdimagno@umich.edu
Abstract:
Nitric oxide (NO) is a gaseous neurotransmitter, a vasodilator and paracrine regulator. In the pancreas, NO regulates normal pancreatic exocrine secretion, endocrine pancreatic insulin secretion and pancreatic microvascular blood flow. NO has multiple species and is produced de novo by 3 NO synthase enzymes. Endothelial NO synthase reduces the severity of the initial phase of experimental acute pancreatitis (AP). Cigarette smoking and chronic alcohol use disrupt normal NO pathways and are associated with pancreatitis and pancreatic cancer. The aims of this minireview are to describe normal intrapancreatic NO pathways, perturbations during experimental AP and due to epidemiological factors associated with pancreatic pathology, and the clinical implications of NO on AP.
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Acute Pancreatitis II: Pathophysiology
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Acute Pancreatitis I: Introduction
Acute pancreatitis is characterized by rapid inflammation of the pancreas, often caused by factors like gallstone blockage or excessive alcohol consumption. Chronic pancreatitis, on the other hand, is a slow, progressive inflammation that may result from long-term alcohol abuse, obstructions in the pancreatic duct, or genetic factors.
The causes of acute pancreatitis include:
Acute Pancreatitis I: Introduction
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