“…Various mechanisms have been suggested to explain the effects of IPC, such as activation of adenosine, adrenergic, bradykinin, and opioid receptors, activation of intracellular mediators such as protein kinase C , tyrosine kinases and the adenosine triphosphate (ATP)-sensitive potassium channels in the mitochondria1 membrane, expression of heat shock proteins, synthesis of antioxidant enzymes, and many others [30,31,321. However, there is still an ongoing discussion as to whether these effects represent causes, effects, or just epi-phenomena There is a high level of evidence that microcirculatory derangement caused by I/R injury plays a pivotal role in the pathogenesis of pancreatitis [33,34,35,36,371. Structural and functional damage in I/R injury results in leukocyte accumulation and adherence to venules, platelet aggregation, vasoconstriction and deterioration of capillary perfusion, which can be quantified by intravital fluorescence microscopy [38].…”