title: [Postconditioning -- effective method against distant organ dysfunction?].
abstract: BACKGROUND
  The ischemia-reperfusion injury of the small intestine is a condition of high mortality, which occurs following superior mesenteric artery (SMA) embolization or circulatory redistribution. The aim of the study was to evaluate the local and systemic effects of postconditioning in a rat model of small intestine ischemia-reperfusion.
  
  
  METHODS
  Male Wistar rats underwent 60 min ischemia by the clamping of the SMA, followed by 6 hrs of reperfusion. The animals (n = 30) were randomized into three groups: sham-operated, control-, and postconditioned. Postconditioning was performed at the very onset of reperfusion by 6 alternating cycles of 10-10 seconds reperfusion/reocclusion, for a total of 2 min. At the end of the reperfusion blood and tissue (small intestine, lungs, kidney, liver) samples were taken for histological examination. The antioxidant status of small intestine was measured from intestinal homogenates.
  
  
  RESULTS
  Histologic results revealed increased damage in control-group lungs, kidney, liver and small intestine in comparison with the postconditioned group. The injury was supported by significantly higher wet/dry weight ratio (p = 0.026), and serum levels of creatinine (p = 0.013), ASAT (p = 0.038), LDH (p = 0.028) and CK (p = 0.038) in the control group. The postconditioned group showed lower serum IL-6 levels (420 pg/ml vs. 188 pg/ml), as well as significantly higher mucosal antioxidant concentration.
  
  
  CONCLUSIONS
  Postconditioning was able to decrease not only local, but the systemic damage intensity also, after a small intestinal ischemic-reperfusion episode.
authors.affiliation: Semmelweis Egyetem, Általános Orvostudományi Kar I. sz. Sebészeti Klinika 1082 Budapest Üllői út 78. peter.onody@gmail.com
authors.forename: Péter
authors.initials: P
authors.lastname: Onody
authors.forename: Olivér
authors.initials: O
authors.lastname: Rosero
authors.forename: Tibor
authors.initials: T
authors.lastname: Kovács
authors.forename: Dávid
authors.initials: D
authors.lastname: Garbaisz
authors.forename: Viktor
authors.initials: V
authors.lastname: Hegedüs
authors.forename: Gábor
authors.initials: G
authors.lastname: Lotz
authors.forename: László
authors.initials: L
authors.lastname: Harsányi
authors.forename: Attila
authors.initials: A
authors.lastname: Szijártó
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D015415:Biomarkers / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D003404:Creatinine / Q000097:blood; D004797:Enzyme-Linked Immunosorbent Assay; D007421:Intestine, Small / Q000473:pathology* / Q000503:physiopathology*; D057775:Ischemic Postconditioning / Q000379:methods; D007633:Keratins / Q000097:blood; D007668:Kidney / Q000473:pathology / Q000503:physiopathology; D008099:Liver / Q000473:pathology / Q000503:physiopathology; D008168:Lung / Q000473:pathology / Q000503:physiopathology; D008297:Male; D017538:Mesenteric Artery, Superior / Q000503:physiopathology; D009929:Organ Size; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000209:etiology / Q000473:pathology / Q000503:physiopathology* / Q000517:prevention & control*
chemical_list: D015415:Biomarkers; D008076:Cholesterol, HDL; D007633:Keratins; D003404:Creatinine; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase