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Early organ-specific mitochondrial dysfunction of jejunum and lung found in rats with experimental acute pancreatitis

2011; Elsevier BV; Volume: 13; Issue: 5 Linguagem: Inglês

10.1111/j.1477-2574.2010.00290.x

1477-2574

Anubhav Mittal, Anthony J. Hickey, Chau C. Chai, Benjamin Loveday, Nichola M. Thompson, Anna Dare, Brett Delahunt, Garth J. S. Cooper, John A. Windsor, Anthony R.J. Phillips,

Liver Disease Diagnosis and Treatment

IntroductionMultiple organ dysfunction is the main cause of death in severe acute pancreatitis. Primary mitochondrial dysfunction plays a central role in the development and progression of organ failure in critical illness. The present study investigated mitochondrial function in seven tissues during early experimental acute pancreatitis.MethodsTwenty-eight male Wistar rats (463 ± 2 g; mean ± SEM) were studied. Group 1 (n= 8), saline control; Group 2 (n= 6), caerulein-induced mild acute pancreatitis; Group 3 (n= 7) sham surgical controls; and Group 4 (n= 7), taurocholate-induced severe acute pancreatitis. Animals were euthanased at 6 h from the induction of acute pancreatitis and mitochondrial function was assessed in the heart, lung, liver, kidney, pancreas, duodenum and jejunum by mitochondrial respirometry.ResultsSignificant early mitochondrial dysfunction was present in the pancreas, lung and jejunum in both models of acute pancreatitis, however, the Heart, liver, kidney and duodenal mitochondria were unaffected.ConclusionsThe present study provides the first description of early organ-selective mitochondrial dysfunction in the lung and jejunum during acute pancreatitis. Research is now needed to identify the underlying pathophysiology behind the organ selective mitochondrial dysfunction, and the potential benefits of early mitochondrial-specific therapies in acute pancreatitis.