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Desferrioxamine in warm reperfusion media decreases liver injury aggravated by cold storage

World Journal of Gastroenterology 2013年第5期19卷 673-681页

作者： Peter G Arthur Xian-Wa Niu Wen-Hua Huang bastiaan deboer Ching Tat Lai Enrico Rossi John Joseph Gary P Jeffrey School of Biomedical Biomolecular and Chemical Sciencesthe University of Western AustraliaCrawleyWA 6009Australia School of Medicine and Pharmacology the University of Western AustraliaCrawleyWA 6009Australia Gastroenterology/Hepatology Sir Charles Gairdner HospitalNedlandsWA 6009Australia WA Liver and Kidney Transplantation Services QEII Medical CentreHospital AvenueNedlandsWA 6009Australia Division of Anatomical Pathology PathWestQEII Medical CentreHospital AvenueNedlandsWA 6009Australia Department of Biochemistry Path-WestQEII Medical CentreHospital AvenueNedlandsWA6009Australia

AIM:To evaluate whether desferrioxamine decreases ischemia and perfusion injury aggravated by cold storage(CS)in a rat liver perfusion model. METHODS:Isolated rat livers were kept in CS in University of Wisconsin Solution for 20 h at 4℃,then exposed to 25 min of warm ischemia(WI)at 37℃ followed by 2 h of warm perfusion(WP)at 37℃with oxygenated(95%oxygen and 5%carbon dioxide) Krebs-Henseleit ***(DFO),an iron chelator,was added at different stages of storage,ischemia and perfusion:in CS only,in WI only,in WP only, in WI and perfusion,or in all *** samples were collected after CS and after *** samples and bile were collected every 30 min(0,0.5,1,1.5 and 2 h)during liver *** injury was assessed by the determination of lactate dehydrogenase(LDH) and aspartate aminotransferase(AST)in the effluent and perfusate *** iron was analysed in the perfusate *** WP,the liver was collected for the determination of liver swelling(wet to dry ratio) and liver morphological examination(hematoxylin and eosin staining). RESULTS:Increased CS time caused increased liver dysfunction during *** 2 h of WP,liver injury was indicated by increased release of AST(0.5 h CS:9.4± 2.2 U/g liver vs 20 h CS:45.9±10.8 U/g liver,P<0.05) and LDH(0.5 h CS:59±14 U/g liver vs 20 h CS:297 ±71 U/g liver,P<0.05).There was an associated increase in iron release into the perfusate(0.5 h CS:0.11 ±0.03μmoL/g liver vs 20 h CS:0.58±0.10μmoL/g liver,P<0.05)and reduction in bile flow(0.5 h CS: 194±12μL/g vs 20 h CS:71±8μL/g liver,P<0.05). When DFO was added during WI and WP following 20 h of CS,release of iron into the perfusate was de- creased(DFO absent 0.58±0.10μmoL/g liver vs DFO present 0.31±0.06μmoL/g liver,P<0.05),and liver function substantially improved with decreased release of AST(DFO absent 45.9±10.8 U/g liver vs DFO present 8.1±0.9 U/g liver,P<0.05)and LDH(DFO absent 297±71 U/g liver vs DFO present 56±7 U/g liver,P<0.05),and inc

关键词： Iron chelation Ischemia and perfusion injury Liver Organ preservation Rat

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