title: Delayed energy protection of ischemic preconditioning on hepatic ischemia/reperfusion injury in rats.
abstract: BACKGROUND
  Hepatic ischemia/reperfusion (IR) injuries associated with hepatic resections are unresolved problems in the clinical practice. The aim of this study is to elucidate the effect of ischemic preconditioning (IPC) on the energy charge (EC) and related mechanisms at the late phase of hepatic IR injury.
  
  
  METHODS
  30 Wistar rats were randomly divided into sham, IR and IPC groups. The model of partial hepatic IR was used. The rats were subjected to 60 min hepatic ischemia, pretreated by IPC (10/15 min) or not. After 24 h of reperfusion, serum alanine aminotransferase (ALT), nitrite/nitrate (NOx), malondialdehyde (MDA), hepatic tissue arginase activity, adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP) and EC of the liver were measured.
  
  
  RESULTS
  Liver injury reduced by IPC is measured by liver tissue arginase activity and serum ALT. Tissue NOx levels in rats pretreated with IPC were significantly higher than levels in the IR group (p < 0.001). Tissue levels of MDA in the liver of the IPC group were found to be significantly lower than the levels in the IR group (p < 0.001). ATP and EC levels 24 h after hepatic ischemia in rats pretreated with IPC were higher than the levels in the IR (p < 0.05). All groups had similar ADP and AMP levels in the liver tissues. The IPC procedure significantly reduced the hepatic necrosis (p < 0.001).
  
  
  CONCLUSIONS
  The results of this study demonstrated that pretreatment with IPC improved tissue ATP, EC, and hepatic necrosis at late stages of ischemia reperfusion injury of the liver. Increased nitric oxide, reduced MDA and arginase activity seemed to play a regulatory role in this delayed protective effect of IPC.
authors.affiliation: Department of Biochemistry, Gazi University, Medical Faculty, Ankara, Turkey.
authors.forename: E
authors.initials: E
authors.lastname: Ofluoglu
authors.forename: M
authors.initials: M
authors.lastname: Kerem
authors.forename: H
authors.initials: H
authors.lastname: Pasaoglu
authors.forename: N
authors.initials: N
authors.lastname: Turkozkan
authors.forename: I
authors.initials: I
authors.lastname: Seven
authors.forename: A
authors.initials: A
authors.lastname: Bedirli
authors.forename: T
authors.initials: T
authors.lastname: Utku Yilmaz
mesh_terms: D000244:Adenosine Diphosphate / Q000378:metabolism; D000249:Adenosine Monophosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001119:Arginase / Q000378:metabolism; D004734:Energy Metabolism; D019194:Ischemic Preconditioning / Q000379:methods*; D008099:Liver / Q000378:metabolism* / Q000473:pathology / Q000601:surgery*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009336:Necrosis; D009566:Nitrates / Q000378:metabolism; D009573:Nitrites / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism* / Q000473:pathology / Q000517:prevention & control*; D013997:Time Factors
chemical_list: D009566:Nitrates; D009573:Nitrites; D000249:Adenosine Monophosphate; D008315:Malondialdehyde; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate; D000410:Alanine Transaminase; D001119:Arginase