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Saudi Journal of Kidney Diseases and Transplantation
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Year : 2009  |  Volume : 20  |  Issue : 6  |  Page : 1010-1014
Reduction of the severity of ischemia reperfusion-induced pancreatitis by ischemic pre-conditioning of the liver


Department of Surgery, University of Shiraz Medical Sciences and Health Services, Transplantation Research Centre, Shiraz, Iran

Correspondence Address:
Seyed Mohammad Vahid Hosseini
Department of Surgery, University of Shiraz Medical Sciences and Health Services, Shiraz
Iran
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PMID: 19861862

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Pre-conditioning by brief exposure to ischemia does not only protect the concerned organ against subsequent severe ischemic damage, but also has protective effect on other organs, which is called remote pre-conditioning. Our aim in this study was to evaluate the protective effect of brief liver ischemia on the pancreas against severe ischemia-reperfusion-induced pancreatitis. This study was performed on 30 male wistar rats. Ischemic pre-conditioning of liver was performed by first clamping of the hepatic pedicle for 10 minutes. Following this, ischemia-reperfusion of the pancreas was performed by first clam-ping the inferior splenic artery for 30 minutes, followed by reperfusion for one hour. The rats were divided into three groups (10 rats in each group). Group­One was the sham operated group, without clamping of any artery. Group-two developed ischemia­reperfusion-induced pancreatitis, without ischemic pre-conditioning of the liver, while Group-three underwent ischemic pre-conditioning of the liver followed by ischemia-reperfusion of the pancreas. Ischemic pre-conditioning, applied prior to induction of pancreatitis, caused a reduction in plasma lipase, plasma interleukin-1β and histological signs of pancreatic damage, but plasma interleukin-10 levels were not significantly different between the three groups. Ischemic pre-conditioning of the liver did not cause any alteration of the liver enzymes. Our study suggests that ischemic pre­conditioning of the liver reduces the severity of ischemia-reperfusion-induced pancreatitis. These effects are partly related to the reduction of pro-inflammatory interleukin -1β.


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