EFFECTS OF LEUKOCYTE AND PLATELET DEPLETION ON ISCHEMIA - REPERFUSIONINJURY TO DOG PANCREAS

Background/Aims: Ischemia-reperfusion injury has been studied in vario us organs. Effects of leukocyte and platelet depletion on ischemia-rep erfusion injury were evaluated using the isolated, perfused dog pancre as in vivo. Methods: Pancreatic exocrine and endocrine functions were stimulated by an intra-arterial injection of cholecystokinin (10(-12) mol) and intravenous injection of glucose and arginine (1 g/kg body wt ), respectively. The functions before and after 60 minutes of ischemia were evaluated in the no treatment and in the leukocyte and platelet depletion groups. Results: Cholecystokinin increased prostaglandin I-2 and thromboxane A(2) production and stimulated exocrine pancreatic se cretion. Glucose and arginine stimulated insulin and glucagon release from the pancreas. Sixty minutes of ischemia followed by 60 minutes of reperfusion damaged the pancreatic acinar and ductular cells. Ischemi a of 60 minutes followed by 90 minutes of reperfusion damaged beta cel ls. Removal of leukocytes (97.6%) and platelets (99.4%) by using a fil ter throughout the experiment prevented the ischemia-reperfusion injur y, reduced plasma lipid peroxide and thromboxane A(2), and increased p rostaglandin I-2 levels. Conclusions: Leukocytes and platelets seem to damage the pancreas during ischemia-reperfusion by increasing the per oxidation of structurally important cell membrane lipids and reduced t he thromboxane A(2) prostaglandin I-2 ratio, a predictor of cellular i njury.