For example, we gave 5 ml of SC normal saline for resuscitation at the start of the protocol in the TIP model, and used tissue homogenates rather than isolated mitochondria to avoid any potential risk of mitochondrial extraction stress or http://www.selleckchem.com/products/Enzastaurin.html artefact. The development of novel therapies to prevent the progression of severe acute pancreatitis-associated MODS continues to be frustrated by a clear understanding of key pathophysiology during the early stages of severe acute pancreatitis.9 In the present study we have shown that the early inhibition of mitochondrial respiratory chain complexes is not global but occurs selectively in lung and jejunum during early acute pancreatitis. Failure of these two specific organ systems contributes significantly to the morbidity and mortality associated with severe acute pancreatitis.

4,6,9,34 This early and selective MD seen in the lung and jejunum during the development of acute pancreatitis offers new insights and avenues to pursue in the underlying pathophysiological events during the early phase of acute pancreatitis. Further research is now needed to document the evolution of MD at multiple time points with disease progression, and to investigate if mitochondrial-specific therapies can prevent or aid recovery of lung and jejunal MD.11,13,16 Such an approach has not been considered for the treatment of acute pancreatitis. Conclusions The present study provides the first comprehensive description of mitochondrial function in multiple organs during early acute pancreatitis.

We have identified a previously unrecognised and early organ-selective inhibition of mitochondrial function distant from the primary site of pancreatic inflammatory damage. These data highlight the need for further research to identify the underlying pathophysiology behind the selective MD in these organs, and the potential benefits of early mitochondrial-specific therapies in acute pancreatitis. Funding The present study was supported with funding for salary, consumables and equipment by the Royal Australasian College of Surgeons, the University of Auckland Research Committee, the Maurice & Phyllis Paykel Trust, Auckland Medical Research Council and Lottery Health New Zealand. Conflicts of interest None declared.

Supporting information Additional Supporting Information may be found in the online version of this article: Table S1 Effect of surgery, caerulein-induced mild pancreatitis and taurocholate-induced severe pancreatitis on mitochondrial function (heart, liver, kidney and duodenum) Click here to view.(66K, doc) Please Drug_discovery note: Wiley-Blackwell are not responsible for the content or functionality of any supporting materials supplied by the authors. Any queries (other than missing material) should be directed to the corresponding author for the article.
The clinical presentation of acute pancreatitis (AP) ranges from a mild and local condition to a severe and systemic disease (Van Laethem et al., 1998).