Amylase was measured on a COBAS MIRA analyser

Amylase was measured on a COBAS MIRA analyser Belinostat ptcl (Roche) using a commercial reagent set (Pointe Scientific, Michigan, USA) according to the manufacturer’s instructions. Statistical analysis Statistical analysis was carried out using GraphPad Prism ? version 4.00 for Macintosh (GraphPad Software, San Diego, California, USA). The Mann�CWhitney U-test with a Bonferroni correction was used for the three relevant planned comparisons. A P-value < 0.05 was considered significant. Results All animals survived the study protocols. Both CIP and TIP models produced acute pancreatitis with the expected elevation in serum amylase (Table 1). There was no clinical or biochemical evidence of established MODS being present at this early time point in either model.

The TIP model produced a more severe acute pancreatitis than the CIP model, as shown by the higher histology scores in the TIP group (Table 1). The serum creatinine and electrolyte measurements were unchanged in the CIP group compared with matched controls (saline-control group). The mild nature of the CIP model was also confirmed by the lack of any other biochemical derangement (Table 1). By contrast, the TIP model had a modest systemic derangement in various biochemical parameters (Table 1). Table 1 Diagnostic, histological, and physiological markers of severity in the different experimental groups Effect of acute pancreatitis on the pancreatic mitochondria Pancreatic MD was apparent in both acute pancreatitis models (Table 2), but its pattern differed between the two.

Whereas CIP lead to a significant depression of glutamate oxidation (complex I dysfunction with decreased GM2 and GM3 along with increased (OXP-I/LEAK-I) in the pancreatic tail, it caused only an increase in the OXP-I,II/OXP-I ratio (indicating Complex I dysfunction relative to complex II) in the pancreatic head (Table 2). TIP significantly depressed flux through Complexes I and II in the pancreatic head (Table 2, Fig. 2). TIP induced no significant changes in mitochondrial function in the pancreatic tail in spite of the tail being oedematous. Table 2 Effect of surgery, caerulein-induced mild pancreatitis and taurocholate-induced severe pancreatitis on mitochondrial function (lung, jejunum and pancreas) Figure 2 A summary of the effects of caerulein pancreatitis, sham surgery and taurocholate pancreatitis on the various respiratory chain complexes.

For definitions of LEAK-I through to CCOc see legend for Figure 1. ��-�� represents inhibition of … Effect of anaesthesia and surgery on mitochondrial function The combination of a volatile anaesthetic and GSK-3 surgery depressed respiratory flux through Complex I, Complex II and isolated Complex IV (CCO) in the lung when compared with the non-operated saline control group (Table 2, Fig. 2) thus preventing the investigation of lung MD in the TIP model.

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