With the concept that
ischemia-reperfusion injury may contribute to the pathogenesis of
acute pancreatitis, we have quantitatively analyzed the pancreatic microcirculation of rats during postischemic reperfusion using intravital fluorescence microscopy.
Ischemia to the pancreas of Sprague-Dawley rats (N = 7) was induced by clamping the arteriae gastroduodenalis, lienalis, gastrica sinistra, and gastricae breves for 60 min followed by 120 min of reperfusion. Ischemic conditions were verified by measurement of microvascular
hemoglobin oxygenation using reflection spectrophotometry (n = 9). Postischemic reperfusion was characterized by a significant (P < 0.05) reduction of functional capillary density to approximately 69% of baseline (no reflow). Reperfusion-induced inflammatory response was reflected by a marked increase (100-fold; P < 0.01) of the number of permanently adherent leukocytes in postcapillary venules (reflow paradox). Postischemic reperfusion was further associated with increased serum
lipase activities, and histomorphological analysis revealed alterations, similar as known in acute interstitial
pancreatitis, ie, neutrophil infiltration, interstitial
edema, and hemorrhagic lesions. We, therefore, conclude that
ischemia-reperfusion- associated events, ie, no reflow and reflow paradox, may be considered as trigger mechanisms in the manifestation of distinct types of
acute pancreatitis, in particular posttransplant
pancreatitis.