Primary, ischemic preconditioning (IP) by brief exposure to ischemia has been shown to protect the heart against damage evoked by subsequent severe ischemia. The aim of our study was to evaluate the influence of IP on the development of ischemia/reperfusion-induced pancreatitis (I/R) and pancreatic regeneration, as well as on the pancreatic presence of FGF-2, PDGF and VEGF. Methods: In male Wistar rats, IP of the pancreas was performed by short-term clamping of celiac artery (2 x 5 min). I/R was induced by clamping of inferior splenic artery for 30 min followed by reperfusion. Rats were sacrificed 1, 5, 12 h or 1, 2, 3, 5, 7, 9 and 21 days after the start of reperfusion. Results: Exposure to regular 30-min pancreatic ischemia followed by reperfusion led to the development of acute necrotizing pancreatitis. In I/R-induced pancreatitis, the pancreatic damage reached the maximal value between the first and second day of reperfusion with subsequent regeneration. IP applied prior to I/R caused the reduction in pancreatic damage and accelerated pancreatic regeneration. It was manifested by the reduction in plasma lipase, plasma IL-1beta and histological signs of pancreatic damage, as well as attenuation of I/R-induced reduction in pancreatic blood flow and pancreatic DNA synthesis. Exposure to IP before I/R caused an increased the lobular immunostaining for FGF-2 from 5-12 h and 5-7 day of reperfusion, PDGF-A from 3-5 day of reperfusion and VEGF from 3-7 day of reperfusion. Conclusions: IP reduces pancreatic damage and accelerates pancreatic healing in the course of I/R-induced pancreatitis. This effect is accompanied by an increase in the pancreatic lobular presence of FGF-2, VEGF and PDGF-A in early stage of pancreatic regeneration suggesting the involvement of these factors in healing-promoting effects of IP.

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