Abstract 14612: Treatment of Ischemia/Reperfusion Injury Through Supplementation With Sodium Selenite: Modification of Oxidative Organ Damage and Inflammatory Response
Introduction: Ischemia/reperfusion (I/R) injury leads to oxidative damage which contributes to the mortality of cardiopulmonary bypass (CPB). Supplementation of Sodium Selenite (Se) is known to induce selenoproteins and thus to counteract oxidative damage. The aim of this study was to investigate the impact of dietary selenium on markers of oxidative tissue damage and inflammation during CPB and deep hypothermic circulatory arrest (DHCA).
Methods: Male rats (Wistar, 400-500g) were fed Se-supplemented chow for 5 weeks (1000μg Se/kg, n=7). Control group (n=7) were fed a Se-adequate diet with 300μg Se/kg. The rats were cannulated for CPB, connected to a heart-lung-machine and cooled down. At 17°C, CPB was interrupted for 45 minutes of DHCA. After rewarming and 60 minutes of reperfusion tissue samples were harvested. Immunoblot analysis was used to detect protein levels of the transcription factor STAT3, the heat shock protein 70 and MAP kinase ERK1/2. Requirement of catecholamine and vital parameters were documented continuously. Activity of the selenoenzyme glutathione peroxidase (GPX) and tissue selenium levels were measured. Serum markers of oxidative tissue damage and inflammation markers were analyzed.
Results: Se-supplementation increased tissue selenium levels as well as GPX-activity and counter-acted I/R-induced ERK1/2 phosphorylation in the heart, while it increased STAT3 phosphorylation and HSP70 expression in the liver. Se-supplemented rats required less catecholaminesubstitution. In addition, Se-supplementation suppressed the I/R-induced increase in ALT, AST, LDH and troponin levels.
Conclusions: According to our data Se-supplementation appears to be effective for prevention of acute I/R-induced tissue damage. The implications of its different actions with regard to oxidative stress markers on recovery after surgery require further investigation.
- © 2013 by American Heart Association, Inc.