Characterization and reduction of ischemia/reperfusion injury after experimental pancreas transplantation

Citation
H. Mayer et al., Characterization and reduction of ischemia/reperfusion injury after experimental pancreas transplantation, J GASTRO S, 3(2), 1999, pp. 162-165
Citations number
21
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Surgery
Journal title
JOURNAL OF GASTROINTESTINAL SURGERY
ISSN journal
1091-255X → ACNP
Volume
3
Issue
2
Year of publication
1999
Pages
162 - 165
Database
ISI
SICI code
1091-255X(199903/04)3:2<162:CAROII>2.0.ZU;2-D
Abstract
Reperfusion injury after pancreas transplantation is a cause of early graft pancreatitis. The aim of this study was to quantify pancreatic microcircul ation after pancreas transplantation in correlation with cold ischemia time . In a second step the effect of N-acetylcysteine on reperfusion damage was tested. Pancreas transplantation was performed in three different-groups o f male Lewis rats. Groups 1 and 2 received no special treatment. Cold ische mia time was 1.5 hours in group 1 and 16 hours in groups 2 and 3. In group 3 donor and recipient were both treated with N-acetylcysteine (300 mg/kg) 1 .5 hours after reperfusion graft microcirculation was quantified by means o f intravital microscopy. Rhodamine-labeled leukocytes, fluoroscein isothioc yanate-labeled erythrocytes, and fluoroscein isothiocyanate-albumin were us ed as fluorochromes. After a cold ischemia time of 16 hours, functional cap illary density, erythrocyte velocity, and leukocyte-endothelium interaction were reduced significantly compared to a cold ischemia time of 1.5 hours ( P <0.05). After 16 hours of cold ischemia, treatment with N-acetylcysteine improved all of these parameters (P less than or equal to 0.05). Ischemia/r eperfusion injury after experimental pancreas transplantation is characteri zed by a disturbance of the pancreatic microcirculation exhibiting a correl ation with the duration of cold ischemia. Treatment of donor and recipient with N-acetylcysteine resulted in prevention of cold ischemia-induced micro circulatory disturbance.