• Open Access

Pathophysiology of Acute Pancreatitis: Potential Application from Experimental Models and Human Medicine to Dogs


  • All writing was undertaken at the University of Melbourne, and was not supported by a grant or other funding body

Corresponding author: C. Mansfield, Faculty of Veterinary Science, The University of Melbourne, 250 Princes Highway, Werribee,Victoria, Australia 3030; e-mail: cmans@unimelb.edu.au.


The cellular events leading to pancreatitis have been studied extensively in experimental models. Understanding the cellular events and inciting causes of the multisystem inflammatory cascades that are activated with this disease is of vital importance to advance diagnosis and treatment of this condition. Unfortunately, the pathophysiology of pancreatitis in dogs is not well understood, and extrapolation from experimental and human medicine is necessary. The interplay of the inflammatory cascades (kinin, complement, cytokine) is extremely complex in both initiating leukocyte migration and perpetuating disease. Recently, nitric oxide (NO) and altered microcirculation of the pancreas have been proposed as major initiators of inflammation. In addition, the role of the gut is becoming increasingly explored as a cause of oxidative stress and potentiation of systemic inflammation in pancreatitis.