Effects of dexamethasone on ischemia reperfusion injury following pringle maneuver
Karaman, K.; Tirnaksiz, M.B.; Ulusu, N.; Dincer, N.; Sener, B.; Gulmez, D.; Tandogan, B.; Sokmensuer, C.; Sayek, I.
Hepato-Gastroenterology 58(106): 465-471
2011
ISSN/ISBN: 0172-6390 PMID: 21661414 Document Number: 652371
Hepatic ischemia reperfusion injury induced by Pringle maneuver leads to bacterial translocation, endotoxemia and apoptosis. Our aim was to compare the effects of low and high dose dexamethasone pretreatment on antioxidant enzyme activities, bacterial translocation, endotoxemia and apoptosis, following Pringle maneuver. Thirty-two rats were randomized into four groups; sham, control and two treatment groups; low dose dexamethasone (0.1 mg/kg) and high dose dexamethasone (1 mg/kg). In the treatment groups dexamethasone was administered intraperitoneally one hour before Pringle maneuver. Twenty-four hours after closing rats' abdomen, re-laparotomy was performed and tissue samples were taken from the mesenteric lymph nodes, liver, ileum and spleen and 1 mL of blood was drawn from the aorta. Bacterial translocation, endotoxemia, apoptosis and enzyme activities of G6PD, 6-PGD, GR, GST, GPx and CAT were evaluated. Low dose dexamethasone significantly decreased bacterial translocation to mesenteric lymph nodes, and reduced liver and enterocyte apoptosis, whereas high dose dexamethasone caused only a significant reduction in enterocyte apoptosis (p<0.05). Dexamethasone both in low and high doses significantly reduced the decrease in antioxidant enzyme levels (p<0.05). Low dose dexamethasone pretreatment caused constructive therapeutic effects after Pringle maneuver, whereas these effects were seen partially with a high dose.