Microcirculatory Disturbances in the Pathogenesis of Acute Pancreatitis

摘要: In acute pancreatitis, reductions in blood flow and alterations of microvascular integrity resulting impaired tissue oxygenation play an important part the progression possibly initiation disease. Independently initial noxa, intra-pancreatic activation trypsinogen to trypsin is crucial trigger pancreatitis. The central events for further course are release local mediators (cytokines, vasoactive substances, free oxygen radicals) subsequently development microcirculatory disturbances leukocytes their infiltration into tissue. At present, deterioration microcirculation seen as most pacemaker a necrotizing addition its potentiatory role, severe pancreatic ischemia can pathogenetic role edematous pancreatitis characterized by increased homogeneous microperfusion. experimental shows progredient decrease capillary perfusion despite stable macrohemodynamics. There increasing evidence that alone may be primary cause or exacerbating promotor from clinical studies there was evidence, during cardiopulmonary bypass triggered found up 25% autopsies patients dying after shock. animal models could induced obstruction terminal arterioles. study Mithofer et al. [1] demonstrates, temporary hemorrhagic hypotension rats per se initiates hypothesis, manifestation injury involves ischemia/reperfusion(I/R)-associated events, supported Menger [2], who analyzed postischemic reperfusion use intravital fluorescence microscopy (Fig. 1, 2). this investigation, post-ischemic significant reduction functional density (noreflow) marked increase permanently adherent postcapillary venules (reflow paradox) 3). addition, histomorphological were similar alteration Postischemic has been reported determine outcome I/R injury. Kusterer [3] have demonstrated sodium taurocholate-induced