title: Ischaemic postconditioning reduces peroxide formation, cytokine expression and leukocyte activation in reperfusion injury after abdominal aortic surgery in rat model.
abstract: OBJECTIVE
  We studied the protective effects of ischaemic postconditioning (PS) on ischemia-reperfusion injury of the lower extremities in a rat model of abdominal aortic intervention. We aimed to examine the evoked oxidative stress, cytokine expression and leukocyte activation after revascularisation surgery.
  
  
  METHODS
  Anesthetized animals (48 Whistar rats) underwent a 60 min infrarenal aorta cross-clamping. After the ischaemic period, an intermittent 4 times 15 s reperfusion--15 seconds ischaemic episodes--were applied (ischaemic postconditioning: group PS). Then we started a 120 min reperfusion in the aorta. In untreated group animals underwent a long ischaemia (60 min) and the following reperfusion (group IR). Peripherial blood samples were collected before operation, and in early (5, 10, 15, 30, 60 and 120 min) reperfusion periods. Serum peroxide level, TNF-alpha concentration, myeloperoxidase (MPO) activity and PMA-induced leukocyte ROS production were measured.
  
  
  RESULTS
  In PS group, plasma peroxide level elevation was significantly lower in very early reperfusion (5-30 min) comparing to non-conditioned IR group (10.04+/-1.9 microM/l vs. 16.91+/-3.67 microM/l, p<0.05). PS also reduced serum TNF-alpha concentration (167.41+/-31.26 microg/ml vs. 116.55+/-12.04 microg/ml, p<0.05), MPO activity (1.759+/-0.239 microM/ml vs. 1.22+/-0.126 microM/ml, p<0.05) and leukocyte activation detected by PMA-induced leukocyte ROS production (5.7+/-0.96 AU/10(3) cells vs. 4.63+/-0.69 AU/10(3) cells).
  
  
  CONCLUSIONS
  Ischaemic postconditioning could reduce ROI production after IR in early reperfusion period, thus limiting ROI mediated tissue lesion, cytokine-leukocyte activation and inflammatory responses. PS seems to be an effective tool in vascular surgery to reduce reperfusion injuries after revascularization interventions.
authors.affiliation: Department of General and Vascular Surgery, University of Pecs Medical School, and Department of Anaesthesiology and Intensive Care, Baranya County Hospital, Pecs, Hungary.
authors.forename: L
authors.initials: L
authors.lastname: Sínay
authors.forename: M
authors.initials: M
authors.lastname: Kürthy
authors.forename: Sz
authors.initials: S
authors.lastname: Horváth
authors.forename: E
authors.initials: E
authors.lastname: Arató
authors.forename: M
authors.initials: M
authors.lastname: Shafiei
authors.forename: J
authors.initials: J
authors.lastname: Lantos
authors.forename: S
authors.initials: S
authors.lastname: Ferencz
authors.forename: A
authors.initials: A
authors.lastname: Bátor
authors.forename: B
authors.initials: B
authors.lastname: Balatonyi
authors.forename: Zs
authors.initials: Z
authors.lastname: Verzár
authors.forename: B
authors.initials: B
authors.lastname: Süto
authors.forename: L
authors.initials: L
authors.lastname: Kollár
authors.forename: Gy
authors.initials: G
authors.lastname: Wéber
authors.forename: E
authors.initials: E
authors.lastname: Roth
authors.forename: G
authors.initials: G
authors.lastname: Jancsó
mesh_terms: D000818:Animals; D001012:Aorta, Abdominal / Q000378:metabolism* / Q000473:pathology / Q000601:surgery*; D005260:Female; D005786:Gene Expression Regulation; D019194:Ischemic Preconditioning; D007962:Leukocytes / Q000378:metabolism* / Q000473:pathology; D008297:Male; D010545:Peroxides / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism* / Q000473:pathology / Q000601:surgery; D013997:Time Factors; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis*
chemical_list: D010545:Peroxides; D014409:Tumor Necrosis Factor-alpha